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PROCEEDINGS

13th TNS CONFERENCE 2007 THE THIRTEENTH ANNUAL CONFERENCE OF THE

THAI NEUROSCIENCE SOCIETY JULY 28-29, 2007

IN CONJUNCTION WITH

9th IBRO-APRC ASSOCIATE NEUROSCIENCE SCHOOL

JULY 22-27, 2007

PHITSANULOK, THAILAND

Organized by

The Thai Neuroscience Society Faculty of Science, Mahidol University

Faculty of Medical Science, Naresuan University Commission of Higher Education, Ministry of Education

International Brain Research Organization

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WELCOME Dear Participants

On behalf of the Organizing Committee, it is my great pleasure to welcome you to the Thirteenth Annual Conference of the Thai Neuroscience Society. This conference is jointly organized by the Faculty of Science, Mahidol University, the Faculty of Medical Science, Naresuan University and the Thai Neuroscience Society. Conferences, such as these, provide us with an opportunity to come together and share our findings and information, research experiences and new discoveries in the field of neuroscience, and bring about progress in science and technology, thereby improving the quality of life for people. In addition we hope that cordial relationships and close cooperation will develop among those in attendance.

This year, the 13th TNS Conference 2007 is a part of the 9th IBRO-APRC Associate Neuroscience School. The International Brain Research Organization (IBRO) Asia-Pacific Regional Committee (APRC) made a decision to support the organization of an Associate School in Thailand. The purpose of the IBRO-APRC Associate School is to introduce updated concepts of neuroscience to junior graduate students (e.g. those in their junior PhD year or in the 2nd year MSc course) in under-privileged regions. Another aim of the Associate School is to identify bright students who are suitable to attend the main Neuroscience Schools in different parts of the Asia-Pacific region or even the RIKEN Summer School (Wako, Japan) within the next couple of years. Funding from IBRO and Thai Neuroscience Society will enable about 30 students to attend this 5-day School. This also provides a forum for young neuroscientists, especially those from developing countries, to be exposed to high quality neuroscience. IBRO students will also present their own research work in this Conference. We would like to take this opportunity to thank the IBRO Asian Pacific Regional Committee who has supported the Thai Neuroscience Society to organize the 9th IBRO-APRC Associate Neuroscience School in Bangkok. We are especially grateful for the attendance of the overseas teachers who traveled great distances from different countries, viz. Canada, Japan, Malaysia, UK and USA. I sincerely hope that everyone will gain the maximum benefit from this Conference. May I take this moment to extend a warm welcome to all delegates, especially to our guests from abroad. I wish you a very pleasant stay in Thailand. Thank you. Associate Professor Dr. Sukumal Chongthammakun Chairman of the Organizing Committee the 9th IBRO-APRC Associate Neuroscience School and the 13th TNS Conference 2007

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Distinguished Guests, Ladies and Gentlemen

I am honored and delighted to have the opportunity to make an opening remark on the occasion of the opening ceremony of the Thirteenth Annual Conference of the Thai Neuroscience Society, 2007.

On behalf of the Thai Neuroscience Society, I have the privilege of welcoming you to the Thirteenth Annual Conference of the Thai Neuroscience Society, 2007.

As you know, research in neuroscience contributes significantly to society by increasing our understanding of the brain, its organization and function. Knowledge generated by neuroscience research has led to important advances in the understanding of diseases and disorders that affect the nervous system and to the development of better treatments which reduce suffering. Since neuroscience comprises several fields, for example, neuroanatomy, neurophysiology, neurochemistry, neuropharmacology, neuropsychology and neuronal modeling. The cross-disciplinary training and interacting in neuroscience is becoming of paramount importance. This conference is filled with interesting and exciting papers in various fields of neuroscience. Some of these papers are contributed by the young neuroscientists from the Asian Pacific Region, including Thais. Many of them are the IBRO fellowship recipients. These IBRO students are selected for the Neuroscience School in Bangkok, based on the basis of academic record and written statements concerning both their interest in neuroscience and their expectation of the School. I believe that the interactions among these young neuroscientist in this conference will help to stimulate the development of neuroscience in this region and facilitate the collaborative research network in the future.

Finally, I would like to thank the Organizing Committee for their hard work, especially individuals from the Faculty of Science, Mahidol University and the Faculty of Medical Science, Naresuan University. I would like to thank the IBRO Asian Pacific Regional Committee for the major support on the 9th IBRO-APRC Associate Neuroscience School in Thailand. I would now like to declare open this 13th TNS Conference 2007 and wish you all a very fruitful and enjoyable meeting. Thank you. Professor Dr. Pavich Tongroach President, FAONS & Thai Neuroscience Society

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Organizing Committee of the 9th IBRO-APRC Associate Neuroscience School

and the 13th TNS Conference 2007 Advisory Committee:

Pavich Tongroach President of FAONS and Thai Neuroscience Society

Mondhon Sanguansermsri President of Naresuan University Amaret Bhumiratana Dean, Faculty of Science,

Mahidol University Chairperson:

Sukumal Chongthammakun General Secretary:

Thongchai Sooksawate

Members of the Organizing Committee:

Anan Srikiatkajorn

Banthit Chetsawang

Boonyong Tantisira

Chainarong Tocharas

Ittipon Phoungpetchara

Jintanaporn Watanatorn

Jiraporn Tocharas

Kanokwan Tilokskulchai

Kittisak Sripanichkulchai

Mayuree Tantisira

Naipinich Kotchabhakdi

Niwat Taepavarapruk

Nuanchan Jutapakdeekul

Onrawee Khongsombat

Pansiri Phansuwan

Piyarat Govitrapong

Pornnarin Taepavarapruk

Sukkid Yasothornsrikul

Supin Chompoopong

Sutisa Nudmamud Thanoi

Vilai Chentanez

Yupin Sanvarinda

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Conference Venue: Faculty of Medical Science, Naresuan University

Phitsanulok 65000, Thailand Registration Saturday, July 28, 2007 08.30-12.00 Sunday, July 29, 2007 08.30-12.00 Opening Ceremony Saturday, July 28, 2007 09.00-09.30 Keynote Lecture Saturday, July 28, 2007 09.30-10.15

Anthony Phillips, University of British Columbia, Canada “Functional Correlates of Long-Term Depression of Excitatory Synapses”

Plenary Lecture Saturday, July 28, 2007 10.30-14.30

John Schetz, UNTHSC, USA. “Structural Microdomains Pivotal for the Selective Interaction of Ligands and Activation of Dopamine Receptors”

Gavin Reynolds, Queen University, United Kingdom.

“The Neurotransmitter Pathology of Schizophrenia” Norman Scholfield, Queens University, United Kingdom.

“The Role of Arteriolar Dysfunction to Diabetic Retinopathy” Sunday, July 29, 2007 09.00-09.45

Piyarat Govitrapong, Mahidol University, Thailand. “Melatonin Attenuates Amphetamine-Induced Neurotoxicity in the Experimental Model of Parkinson's Disease”

Special Lecture Sunday, July 29, 2007 09.45-14.00

Sukkid Yasothornsrikul, Naresuan University, Thailand. “Proteases in Neuroendocrine System: A New Look”

Niwat Taepavarapruk, Naresuan University, Thailand.

“State-Dependent GABAergic and Glycinergic Controls on the Sensory Transmission through the Dorsal Spinocerebellar Tract”

Christopher Ramseyer, Université de Franche-Comté, France.

“Can We Learn Something on Ionic Channel at the Molecular Level that Can Be Transposed to Build Technological Devices?”

Presentation

Oral Presentation: The time allowed for each paper is 15 min including time for discussion. Speakers are requested to leave 3 min for discussion. A computer is available in the conference room. Files should be prepared using Microsoft Powerpoint.

Poster Presentation: The presenters are requested to register their posters at the registration desk. All

posters must be registered and mounted on Saturday, July 28, 2007at 08.30-09.30 and leave in place for the full 2 days. During the presentation time, the presenters are required to attend their own posters. Poster sessions are held on Saturday, July 28, 2007, 14.30-15.30 for the odd posters, and Sunday, July 29, 2007, 10.30-11.30 for the even posters. You should present your abstract for one hour during the session period, beginning at presentation time shown above. All posters must be removed after the closing ceremony.

One poster will be selected based on the votes of the conference participants. The voting deadline is 16.30 on Saturday, July 28, 2007. The winners’ names will be announced and the prize-winner will be awarded at the closing ceremony.

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Program 13th TNS Conference 2007

July 28-29, 2007 Naresuan University, Phitsanulok, Thailand

Saturday 28 July 2007 08.30-09.00 Registration 09.00-09.30 Opening Ceremony:

Welcome Remarks by Prof. Pavich Tongroach, President of Thai Neuroscience Society, Thailand

Opening Remarks by Assoc. Prof. Mondhon Sanguansermsri, President of Naresuan University, Thailand

09.30-10.15 Keynote Lecture:

Functional Correlates of Long-Term Depression of Excitatory Synapses Prof. Anthony Phillips, University of British Columbia, Canada

10.15-10.30 Refreshments 10.30-11.15 Plenary Lecture 1:

Structural Microdomains Pivotal for the Selective Interaction of Ligands and Activation of Dopamine Receptors

Dr. John Schetz, UNTHSC, USA 11.15-12.00 Oral Presentation 1: Chairperson: Assoc. Prof. Boonyong Tantisira

11.15 High Frequency Stimulation of the Periaqueductal Gray Matter & Ventromedial

Hypothalamus: Amplitude and Frequency Modulation and Regional Brain c-Fos Activation

Lim Lee Wei

11.30 Expression of Recombinant Mouse Estrogen Receptor(ER) β-ligand Binding Domain (LBD) and Its Interaction with Nuclear Proteins of Mouse Brain

Paramanik Vijay and Thakur MK

11.45 Effect of CF1 on Object Recognition and Spatial Navigation In Rat Wipawee Boongvang, Jintanaporn Wattanathorn, Supaporn Muchimapura, Siriporn Tiamkao , Chuleratana Banchonglikitkul and Taweesak Suntorntanasas

12.00-13.00 Lunch 13.00-13.45 Plenary Lecture 2:

The Neurotransmitter Pathology of Schizophrenia Dr. Gavin Reynolds, Queens University, UK

13.45-14.30 Plenary Lecture 3:

The Role of Arteriolar Dysfunction to Diabetic Retinopathy Dr. Norman Scholfield, Queens University, UK

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14.30-15.30 Refreshments and Poster Presentation 1 15.30-16.30 Oral Presentation 2: Chairperson: Assoc Prof. Pansiri Pansuwan

15.30 Screening Effect of Zingiber Officinale Extract on Cognitive Function in Male Rats

Jinatta Jittiwat, Jintanaporn Wattanathorn, Terdthai Tong-un, Supaporn Muchimapura and Kornkanok Ingkaninan

15.45 Neuroprotective Effect of Bacopa monnieri in Various Brain Areas.

Nongnut Uabundit, Jintanaporn Wattanathorn, Supaporn Muchimapura and Kornkanok Ingkaninan

16.00 Effects of Semi-Chronic Ethanol Consumption on the Cerebellar Dentate

Nucleus: A Quantitative Study in the Rats Wang T.C. and Kotchabhakdi N.

16.15 Differential Circadian Regulation of Clock Genes in the Hamster Pineal Gland

Wongchitrat, P, Simonneaux, V, Felder-Schmidt, MP, Pévet, P, Govitrapong, P and Phansuwan-Pujito, P

16.30-17.30 TNS Annual Business Meeting 18.30 Welcome Reception Sunday 29 July 2007 09.00-09.45 Plenary Lecture 4:

Melatonin Attenuates Amphetamine-Induced Neurotoxicity in the Experimental Model of Parkinson's Disease

Prof. Piyarat Govitrapong, Center for Neuroscience, Faculty of Science, Mahidol University, Thailand.

09.45-10.30 Special Lecture 1:

Proteases in Neuroendocrine System: A New Look Dr. Sukkid Yasothornsrikul, Faculty of Medical Science, Naresuan University, Thailand.

10.30-11.30 Refreshments and Poster Presentation 2 11.30-12.15 Special Lecture 2:

State-Dependent GABAergic and Glycinergic Controls on the Sensory Transmission through the Dorsal Spinocerebellar Tract

Dr. Niwat Taepavarapruk, Faculty of Medical Science, Naresuan University, Thailand.

12.15-13.15 Lunch 13.15-14.00 Special Lecture 3:

Can We Learn Something on Ionic Channel at the Molecular Level that Can Be Transposed to Build Technological Devices?

Dr. Christopher Ramseyer, Faculté des Sciences, Université de Franche-Comté, France.

14.00-15.00 Certificate Presentation and Closing Ceremony 15.00-15.30 Refreshments

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POSTERS

PP 1: Possible GABAergic Modulatory Effect of Allopregnanolone in Sleep Deprivation–Induced Anxiety like Behavior and Oxidative Damage in Mice

Anant Singh and Anil Kumar PP 2: Effect of Paraoxon on GABA Uptake by Rat Hippocampal Synaptosomes

Fereshteh Poorabdolhossein, Asghar Qasemi, Ameneh Shahrokhi, Ali Khoshbaten and Alireza Asgari

PP 3: Protective Effect of Zolpidem in Acute Immobilization Stress–Induced Certain Behavior

and Biochemical Alterations in Mice and Its Possible GABAergic Mechanism Richa Goyal and Kumar Anil

PP 4: Spinal Cord Injury Induced Oxidative Stress: Role of 3-Aminobenzamide

Sankar Venkatachalam, Vijaya Prakash, Krishnan Muthaiah, Tamilselvi Palaniappan and Sridhar Skylab

PP 5: Role of Oxidative Stress in Mitochondrial Dysfunctions and Behavioral Alterations in

Rat Following Chronic Carbofuran Exposure Sukhdev Singh Kamboj, Vikas Kumar, Amit Kamboj and Rajat Sandhir

PP 6: Protective Effect of Carvedilol on 3-Nitropropionic Acid Induced Behavioral Alterations

and Oxidative Stress in Rats Puneet Kumar, Padi SSV, Naidu PS and Kumar Anil

PP 7: Protective Effect of Minocycline, A Semi-Synthetic Second-Generation Tetracycline

against 3-Nitropropionic Acid -Induced Neurotoxicity Manuj Ahuja, Mahendra Bishnoi and Kanwaljit Chopra

PP 8: Effect of Electrical Lesion of Amygdala Basolateral-Lateral Nuclei on the Piriform

Cortex Kindled Seizures in Rats P Shahabi, SJ Mirnajafi-Zadeh, Y Fathollahi, N Hosseinmardi, ME Rezvani, A Eslamifar and Z Deljou

PP 9: Involvement of Adenosinergic Receptors in Mediating the Anti-Epileptic Action of

Rofecoxib (A Selective COX-2 Inhibitor) in Mice Kiran Kumar Akula, Ashish Dhir and S.K.Kulkarni

PP 10: Role of Diet in the Therapy of Epilepsy in Traditional Persian Medicine

Parinejad N. and Raza M. PP 11: Maternal Micronutrient Deficiency Modulates the Expression and Activity of Fetal Brain

NMDA Receptor and Per Se Alters the Offspring Cognitive Functions Rosario JF and Patrick Gomez M

PP 12: Effects of Ascorbic Acid on Streptozotocin Induced Oxidative Stress and Memory

Impairment in Rats Weerateerangkul, P

PP 13: Regional Differences in Microglial Susceptiblity to Amyloid Beta in the Rat Brain

Prabhakar Singh and Taposh Kumar Das PP 14: Protective Effects of N-(2-Propylentanoyl) Urea on CA1 and CA3 Neuronal Cell Death

after Common Carotid Arteries Occlusion in Mice Oraphan Wanakhachornkrai, Boonyong Tantisira and Mayuree H. Tantisira

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PP 15: Screening of Indian Herbal Medicine in the Treatment of Alzheimer's Disease P. Levin Michel Anbu Gomez

PP 16: Effects of Thai Traditional Herbal Formulas (Yahom) on the Central Nervous System

Aree Wanasuntronwong, Boonyong Tantisira and Mayuree H. Tantisira PP 17: Effect of Persistent Pain on the Synaptic Transmission in Hippocampal Formation

Ya-li Long, KE-RUI GONG, Ming-gang Liu, Zhen LI, Xiao-yan Zhao, Cui-ying Gao, Xue-feng Chen, Rui-rui Wang, Yong Xiao, Xiu-yu Cui,Hua Li,Yang-yuan An, Lan-feng Zhao and Jun Chen

PP 18: Involvement of MAPK Pathway in the Generation and Maintenance of Bone Cancer

Pain Li Tingting, Zhao Zhiqi, Ji Rurong and Zhang Yuqiu

PP 19: Electrical Stimulation on the Denervated Muscle Attenuates Neuropathic Pain after

Spared Nerve Injury Supin Chompoopong, Kanyarat Bamrungsuk, Kanokwan Tilokskulchai

PP 20: Cisplatin-Induced Neuropathy in the Rat Model: Differences between Genders

Tulaporn Wongtawatchai, Sithiporn Agthong and Vilai Chentanez PP 21: Protective Effects of Centrophenoxine, an Antiaging and Antioxidant Drug, against

Rotenone Induced Parkinson Disease Ranjeet Verma and Bimla Nehru

PP 22: The Neuroprotective Effect of Melatonin and Monoamine Uptake Blocker on SH-SY5Y

Dopamine Cell Line Chutikorn Nopparat, Piyarat Govitrapong and Banthit Chetsawang

PP 23: The Effects of Genistein on Okadaic Acid-Induced Hyperphosphorelated Tau Protein in

SH-SY5Y Cells In Vitro Siriporn Chamniansawat and Sukumal Chongthammakun

PP 24: Signaling Pathway in Methamphetamine-Induced tPA Gene Expression

Kanchanat Ternchoocheep and Sukkid Yasothornsrikul PP 25: Polymorphism of Glutamate N-Methyl-D-Aspartate Receptor Subunit 2B in

Methamphetamine Abusers Rachanee Chanasong, Samur Thanoi, Paritat Watiktinkorn and Sutisa Nudmamud-Thanoi

PP 26: Phosphorylation of cAMP Response Element Binding Protein Induced by Group I

Metabotropic Glutamate Receptors in Astrocytes : Prelimainary Studies Kittikun Viwatpinyo and Sukumal Chongthammakun

PP 27: Different Effects of Naloxone on Sweet Food Intake of Repeated Restraint-Stress Rat

and Non-Stress Rat Suwaporn Daendee, Sarinee Kalandakanond-Thongsong and Sutthasinee Poonyachoti

PP 28: Localization of Delta Opioid Receptors in Efferent Nerve Fibers of the Rat Cochlear

Kwankanit Saeung, Pansiri Phansuwan-Pujito, Stefano Casalloti, Andrew Forge and Piyarat Govitrapong

13TH TNS CONFERENCE JULY 28-29, 2007 PHITSANULOK, THAILAND

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CONTENTS PLENARY LECTURES Functional Correlates of Long-Term Depression of Excitatory Synapses

Anthony Phillips 3 The Neurotransmitter Pathology of Schizophrenia

Gavin Reynolds 5 The Role of Arteriolar Dysfunction to Diabetic Retinopathy

Norman Scholfield 6

Melatonin Attenuates Amphetamine-Induced Neurotoxicity in the Experimental Model of Parkinson's Disease

Piyarat Govitrapong 7 SPECIAL LECTURES State-Dependent GABAergic and Glycinergic Controls on the Sensory Transmission through the Dorsal Spinocerebellar Tract

Niwat Taepavarapruk 8 Can We Learn Something on Ionic Channel at the Molecular Level that Can Be Transposed to Build Technological Devices?

C. Boiteux, S. Kraszewski, C. Girardet, C. Ramseyer 9 ORAL PRESENTATIONS High Frequency Stimulation of the Periaqueductal Gray Matter & Ventromedial Hypothalamus: Amplitude and Frequency Modulation and Regional Brain c-Fos Activation

Lim Lee Wei 13 Expression of Recombinant Mouse Estrogen Receptor(ER) β-ligand Binding Domain (LBD) and Its Interaction with Nuclear Proteins of Mouse Brain

Paramanik Vijay and Thakur MK 14 Effect of CF1 on Object Recognition and Spatial Navigation In Rat

Wipawee Boongvang, Jintanaporn Wattanathorn, Supaporn Muchimapura, Siriporn Tiamkao, Chuleratana Banchonglikitkul and Taweesak Suntorntanasas 15

Screening Effect of Zingiber Officinale Extract on Cognitive Function in Male Rats

Jinatta Jittiwat, Jintanaporn Wattanathorn, Terdthai Tong-un, Supaporn Muchimapura and Kornkanok Ingkaninan 16

Neuroprotective Effect of Bacopa monnieri in Various Brain Areas.

Nongnut Uabundit, Jintanaporn Wattanathorn, Supaporn Muchimapura and Kornkanok Ingkaninan 17

Effects of Semi-Chronic Ethanol Consumption on the Cerebellar Dentate Nucleus: A Quantitative Study in the Rats

Wang T.C. and Kotchabhakdi N. 18 Differential Circadian Regulation of Clock Genes in the Hamster Pineal Gland

Wongchitrat, P, Simonneaux, V, Felder-Schmidt, MP, Pévet, P, Govitrapong, P and Phansuwan-Pujito, P 19


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POSTER PRESENTATIONS Possible GABAergic Modulatory Effect of Allopregnanolone in Sleep Deprivation–Induced Anxiety like Behavior and Oxidative Damage in Mice

Anant Singh and Anil Kumar 23 Effect of Paraoxon on GABA Uptake by Rat Hippocampal Synaptosomes

Fereshteh Poorabdolhossein, Asghar Qasemi, Ameneh Shahrokhi, Ali Khoshbaten and Alireza Asgari 24

Protective Effect of Zolpidem in Acute Immobilization Stress–Induced Certain Behavior and Biochemical Alterations in Mice and Its Possible GABAergic Mechanism

Richa Goyal and Kumar Anil 25 Spinal Cord Injury Induced Oxidative Stress: Role of 3-Aminobenzamide

Sankar Venkatachalam, Vijaya Prakash, Krishnan Muthaiah, Tamilselvi Palaniappan and Sridhar Skylab 26

Role of Oxidative Stress in Mitochondrial Dysfunctions and Behavioral Alterations in Rat Following Chronic Carbofuran Exposure

Sukhdev Singh Kamboj, Vikas Kumar, Amit Kamboj and Rajat Sandhir 27 Protective Effect of Carvedilol on 3-Nitropropionic Acid Induced Behavioral Alterations and Oxidative Stress in Rats

Puneet Kumar, Padi SSV, Naidu PS and Kumar Anil 28 Protective Effect of Minocycline, A Semi-Synthetic Second-Generation Tetracycline against 3-Nitropropionic Acid -Induced Neurotoxicity

Manuj Ahuja, Mahendra Bishnoi and Kanwaljit Chopra 29 Effect of Electrical Lesion of Amygdala Basolateral-Lateral Nuclei on the Piriform Cortex Kindled Seizures in Rats

P Shahabi, SJ Mirnajafi-Zadeh, Y Fathollahi, N Hosseinmardi, ME Rezvani, A Eslamifar and Z Deljou 30

Involvement of Adenosinergic Receptors in Mediating the Anti-Epileptic Action of Rofecoxib (A Selective COX-2 Inhibitor) in Mice

Kiran Kumar Akula, Ashish Dhir and S.K.Kulkarni 31 Role of Diet in the Therapy of Epilepsy in Traditional Persian Medicine

Parinejad N. and Raza M. 32 Maternal Micronutrient Deficiency Modulates the Expression and Activity of Fetal Brain NMDA Receptor and Per Se Alters the Offspring Cognitive Functions

Rosario JF and Patrick Gomez M 33 Effects of Ascorbic Acid on Streptozotocin Induced Oxidative Stress and Memory Impairment in Rats

Weerateerangkul, P 34 Regional Differences in Microglial Susceptiblity to Amyloid Beta in the Rat Brain

Prabhakar Singh and Taposh Kumar Das 35 Protective Effects of N-(2-Propylentanoyl) Urea on CA1 and CA3 Neuronal Cell Death after Common Carotid Arteries Occlusion in Mice

Oraphan Wanakhachornkrai, Boonyong Tantisira and Mayuree H. Tantisira 36 Screening of Indian Herbal Medicine in the Treatment of Alzheimer's Disease

P. Levin Michel Anbu Gomez 37


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Effects of Thai Traditional Herbal Formulas (Yahom) on the Central Nervous System

Aree Wanasuntronwong, Boonyong Tantisira and Mayuree H. Tantisira 38 Effect of Persistent Pain on the Synaptic Transmission in Hippocampal Formation

Ya-li Long, KE-RUI GONG, Ming-gang Liu, Zhen LI, Xiao-yan Zhao, Cui-ying Gao, Xue-feng Chen, Rui-rui Wang, Yong Xiao, Xiu-yu Cui,Hua Li, Yang-yuan An, Lan-feng Zhao and Jun Chen 39

Involvement of MAPK Pathway in the Generation and Maintenance of Bone Cancer Pain

Li Tingting, Zhao Zhiqi, Ji Rurong and Zhang Yuqiu 40 Electrical Stimulation on the Denervated Muscle Attenuates Neuropathic Pain after Spared Nerve Injury

Supin Chompoopong, Kanyarat Bamrungsuk, Kanokwan Tilokskulchai 41 Cisplatin-Induced Neuropathy in the Rat Model: Differences between Genders

Tulaporn Wongtawatchai, Sithiporn Agthong and Vilai Chentanez 42 Protective Effects of Centrophenoxine, an Antiaging and Antioxidant Drug, against Rotenone Induced Parkinson Disease

Ranjeet Verma and Bimla Nehru 43 The Neuroprotective Effect of Melatonin and Monoamine Uptake Blocker on SH-SY5Y Dopamine Cell Line

Chutikorn Nopparat, Piyarat Govitrapong and Banthit Chetsawang 44 The Effects of Genistein on Okadaic Acid-Induced Hyperphosphorelated Tau Protein in SH-SY5Y Cells In Vitro

Siriporn Chamniansawat and Sukumal Chongthammakun 45 Signaling Pathway in Methamphetamine-Induced tPA Gene Expression

Kanchanat Ternchoocheep and Sukkid Yasothornsrikul 46 Polymorphism of Glutamate N-Methyl-D-Aspartate Receptor Subunit 2B in Methamphetamine Abusers

Rachanee Chanasong, Samur Thanoi, Paritat Watiktinkorn and Sutisa Nudmamud-Thanoi 47

Phosphorylation of cAMP Response Element Binding Protein Induced by Group I Metabotropic Glutamate Receptors in Astrocytes : Prelimainary Studies

Kittikun Viwatpinyo and Sukumal Chongthammakun 48 Different Effects of Naloxone on Sweet Food Intake of Repeated Restraint-Stress Rat and Non-Stress Rat

Suwaporn Daendee, Sarinee Kalandakanond-Thongsong and Sutthasinee Poonyachoti 49

Localization of Delta Opioid Receptors in Efferent Nerve Fibers of the Rat Cochlear

Kwankanit Saeung, Pansiri Phansuwan-Pujito, Stefano Casalloti, Andrew Forge and Piyarat Govitrapong 50


PLENARY AND SPECIAL

LECTURES


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Functional Correlates of Long-Term Depression of Excitatory Synapses Anthony Phillips University of British Columbia, Institute of Mental Health, Vancouver, Canada ABSTRACT

Objective: Long-term synaptic plasticity, including LTP and LTD, at excitatory synapses has been proposed as the cellular substrate of information processing and memory formation in the brain under both physiological and pathological conditions. However, conclusive evidence for a causal relationship between synaptic plasticity and memory is lacking due to the absence of specific drugs that block the expression, the last step, of LTP or LTD without affecting any upstream signaling. The induction of LTD can be inhibited by drugs that block NMDA receptors containing the NR2B subunit. Therefore we have employed selective NR2B antagonists as one strategy to examine the role of LTD various aspects of learning and memory. We have also confirmed that LTD in the hippocampus and nucleus accumbens (NAc) is mediated by a mechanism involving clathrin-mediated and GluR2-dependent endocytosis of postsynaptic AMPARs. On the basis of this finding, we developed a GluR23Y peptide to inhibit the expression of LTD without affecting basal synaptic transmission and other upstream signaling processes involved in the LTD. Using the membrane permeable form of TAT-GluR23Y peptide, we were able for the first time to probe the role of LTD in freely moving rats with unprecedented specificity. This lecture will focus on the role of LTD in the formation and extinction of new behavioral adaptations in conscious animals. Results: 1) The role of hippocampal LTD in acute stress-induced impairment of spatial memory retrieval. Acute stress impairs memory retrieval and facilitates the induction of hippocampal LTD in adult rodents. We found that two structurally distinct inhibitors that specifically prevented either the induction or expression of stress-enabled, NMDA receptor-dependent hippocampal LTD also block the spatial memory retrieval impairments caused by acute stress. Additionally, facilitated induction of hippocampal LTD in vivo, by blocking glutamate transport, mimicked the behavioral effects of acute stress by impairing spatial memory retrieval. Thus, hippocampal LTD is both necessary and sufficient to cause acute stress-induced impairments in spatial memory retrieval and provides a new perspective from which to consider the cognitive deficits in disorders whose symptoms are aggravated by stress. 2) Involvement of LTD in extinction, but not acquisition of conditioned fear memory. Blockade of AMPA receptor endocytosis during initial extinction training disrupted both the expression and consolidation of extinction learning; as did selective blockade of NMDA NR2B receptors with Ro 25-6981. In contrast, administration of Tat-GluR23Y either prior to fear conditioning or during the recall test did not


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affect acquisition or expression of contextual or cue-induced fear. Taken together, these data suggested that AMPA receptor endocytosis is involved specifically in the suppression of a learned fear response during extinction training, but is not involved either in the formation of a new associative memory or the retrieval of an established one. . These data support the hypothesis that LTD may be one synaptic mechanism that facilitates the selective manipulation of an established memory while leaving intact the ability to form new memory. 3) The role of LTD in amphetamine-induced behavioral sensitization. Persistence of drug craving and the strong tendency to relapse are hallmarks of addiction in humans. Drug craving can be modeled in animals as behavioral sensitization of motor activity induced by repeated intermittent administration of drugs of abuse including amphetamine, cocaine, heroin and nicotine. Behavioral sensitization involves neural adaptations in the mesocorticolimbic regions of the brain. Using the membrane permeable TAT- GluR23Y peptide we confirmed that (1) LTD in the NAc in the expression of behavioral sensitization and (2) LTD in the VTA in the induction of behavioral sensitization. Given the links between behavioral sensitization, drug- or cue-induced relapse and craving, these data raise the possibility that treatment with drugs that disrupt LTD may form the basis for a rational drug development strategy for treating addiction-related neuropathology such as craving and relapse to drug-seeking behavior after withdrawal. Supported by grants from NeuroScience Canada and the Canadian Institutes of Health Research.


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The Neurotransmitter Pathology of Schizophrenia Gavin P Reynolds Division of Psychiatry and Neuroscience, Queen’s University Belfast. ABSTRACT

Neuroimaging has identified anatomical and functional abnormalities of the brain in schizophrenia which are reflected by a real, if subtle, neuronal pathology defined by neurochemical and histological findings. Although disturbances of dopaminergic funciton remain implicated by the effects of antipsychotic drugs, there is an accumulation of evidence for abnormalities in both the major neurotransmitter systems of the brain – those of GABA and glutamate. GABAergic neurons can be subdivided according to the calcium binding protein they contain; those containing parvalbumin (PV) and calbindin are diminished in schizophrenia. One of the most substantial abnormalities seen in post-mortem brain tissue is the hippocampal deficit of the PV/GABAergic neurons. This deficit in inhibitory interneurons within structures implicated in schizophrenic symptomatology can be induced by animal models of the disease such as sub-chronic phencyclidine administration or social isolation. The late expression of PV as a protective factor may impart a vulnerability to these neurons early in development, although not possible to identify the timing or aetiological factors associated with this deficit in GABAergic neurons. Nevertheless their association with these animal models suggests an environmental involvement. Neuronal dysfunction determined by MRS measurement of N-acetylaspartate (NAA) deficits in vivo, which we can also assess by NAA analysis in post mortem tissue, is seen in cortical and medial temporal structures in schizophrenia. However reports that NAA deficits increase with time may suggest a progressive pathology of, perhaps, glutamatergic systems. Such loss of glutamatergic function in schizophrenia is supported by decreases in markers for the neuronal glutamate transporter (EAAT3) in striatal structures that receive cortical glutamatergic projections. Deficits in the vesicular glutamate transporter-1 (VGluT) in both striatal and hippocampal regions support this observation, and the association of VGluT density with a genetic risk factor for schizophrenia points to genetic influences on these glutamatergic deficits. Further studies differentiating neuronal loss from diminished activity, and improved models allowing us to determine the temporal and causal relationships between GABAergic and glutamatergic deficits will lead to a better understanding of the processes underlying the neuronal pathology of schizophrenia.


6

The Role of Arteriolar Dysfunction to Diabetic Retinopathy Norman Scholfield Basic Medical Science (Physiology), School of Medicine and Dentistry, Queens University, Medical Biology Centre, Northern Ireland, UK ABSTRACT

Vascular failure is responsible for a large proportion of clinical cases of dysfunction of neural tissue. Diabetes is a disease characterised by numerous secondary complications which are mainly vascular in nature. Diabetic retinopathy is a major cause of blindness and is preceded by failure of vascular autoregulation. Pericyte and arteriolar smooth muscle cell dropout occurs before the loss of microvessels suggesting that dysfunction of these cells are primarily responsible for the pathology. We have assessed the major currents in retinal arteriolar smooth muscle cells and the Ca activated K current (BK) is severely downregulated in diabetes. This study delineates the mechanism of this channel dysfunction and show that Ca release and the alpha subunit of BK are unaffected by diabetes but the beta subunit controlling Ca sensitivity is downregulated. This reduces the hyperpolarising effect of BK channel activation which increases contractile responses thus reducing retinal blood flow.


7

Melatonin Attenuates Amphetamine-Induced Neurotoxicity in the Experimental Model of Parkinson’s Disease Sirirat Klongpanichapak1, Pansiri Phansuwan-Pujito2, Manuchair Ebadi3 and Piyarat Govitrapong 1,4 1Neuro-Behavioural Biology Center, Institute of Science and Technology for Research and Development, Mahidol University, Salaya, Nakornpathom. 2Department of Anatomy, Faculty of Medicine, Srinakharinwirot University, Bangkok, Thailand. 3Department of Pharmacology, Physiology and Therapeutics, School of Medicine and Health Science, University of North Dakota, Grand Forks, ND, USA. 4Center for Neuroscience and Department of Pharmacology, Faculty of Science, Mahidol University, Bangkok, Thailand. ABSTRACT

Amphetamine derivatives are the common drugs of abuse. Chronic or intermittent amphetamine abuse may create temporary or permanent disturbances in dopaminergic systems of the brain that may predispose individuals to Parkinsonism later in life. The study was undertaken to investigate whether amphetamine induced neurotoxicity by affecting systems and pathways which are implicated in Parkinson’s disease (PD). Adult male mice were injected with L-methamphetamine (METH) (30 mg/kg BW, i.p.) for 7 days. These results showed that amphetamine induces nigrostiatal dopaminergic degeneration in mice. The neurotoxicity of D-amphetamine (AMPH) in the human neuroblastoma dopaminergic SK-N-SH cells was further examined. Our data showed that AMPH significantly induced oxidative stress and increased level and aggregation of α-synuclein SK-N-SH cells. Oxidative stress has been proposed as an underlying mechanism responsible for the neurotoxicity. Melatonin, the main secretory product of pineal gland, is well known for its protective effects that are currently attributed mainly to its radical scavenging and antioxidant properties. The study therefore included an investigation of the neuroprotective effects of melatonin against AMPH-induced neurotoxicity in SK-N-SH cells. The present data indicate that the mechanism of AMPH neurotoxicity is involved with oxidative stress and mitochondrial dysfunction and also suggest that the neuroprotective effects of melatonin are, at least in part, associated with its antioxidant properties. Taken together, one may suggest that amphetamine is a risk factor for PD and the use of melatonin could be explored further as a therapeutic approach in PD. Acknowledgements This work was supported by the Thailand Research Fund (TRF) through the Royal Golden Jubilee Ph.D. Program to PG and SK, a Mahidol University Grant and a TRF- Senior Research Scholar Fellowship to PG.


8

State-Dependent GABAergic and Glycinergic Controls on the Sensory Transmission Through the Dorsal Spinocerebellar Tract Niwat Taepavarapruk1, Pornnarin Taepavarapruk1, Shelly A. McErlane2, Anthony G. Phillips3, Joshi John4, Jerome M. Siegel4, and Peter J. Soja2 1Dept. of Physiology, Fac. of Medical Science, Naresuan Univ., Phitsanulok 65000 Thailand. 2Fac. of Pharmaceutical Sciences, Univ. of British Columbia, Vancouver, BC, Canada. 3Dept. of Psychiatry, Univ. of British Columbia, Vancouver, BC, Canada. 4UCLA Dept. of Psychiatry, Neurobiology Research 151A3, VA GLAHS, North Hills California 91343, U.S.A. ABSTRACT

Sleep is a reversible physiological process consisting of a passive, non rapid-eye-movement (NREM) sleep and an active, REM sleep. So far, the neurobiological basis and atypical manifestations of state-dependent control remain poorly understood. The present study, therefore, describes a series of experimental studies designed for investigating the mechanisms underlying somatic sensory modulation during the sleep and wakefulness states. The first set of experiments tested the hypothesis that experimenter-induced synaptic activation of DSCT neurons via, low-intensity stimulation of the sciatic nerve, is state-dependent. By employing chronic single cell recording procedures, we found that low-threshold primary afferent inputs to DSCT neurons mediated by oligosynaptic linkages are reduced during the state of REM sleep. A subsequent eye movement analysis indicates that oligosynaptic input of primary afferent origin to DSCT neurons is specifically suppressed during REM episodes of REM sleep. This result suggests that pre- and postsynaptic inhibitory processes may contribute to the reduced responsivity of DSCT neurons during REM episodes of REM sleep. The second set of experiments tested the hypothesis that GABA and glycine mediate behavioral state specific inhibition of ascending sensory transmission via Clarke’s column DSCT neurons. By using drug microiontophoresis and extracellular unit recording of identified DSCT neurons, we found that REM sleep-specific suppression of both spontaneous and amino acid-driven DSCT cell activities were reversibly blocked by sustained microiontophoretic applications of the GABAA antagonist bicuculline and glycine antagonist strychnine. The third set of experiments tested the hypothesis that the levels of GABA and glycine within Clarke’s column where DSCT neurons were recorded and undergo bicuculline and strychnine-sensitive inhibition during REM sleep also increased during this behavioral state. The technique of microdialysis was employed to sample interstitial fluid from Clarke’s column as a function of sleep and waking states. The results from this study show that the basal levels of glutamate, glycine, GABA and in Clarke’s column significantly increases during REM sleep when compared to NREM sleep or wakefulness. Altogether, we conclude that GABA and glycine mediate behavioral state-specific inhibition of ascending sensory transmission via Clarke's column DSCT neurons. Acknowledgements: This work was supported in part by National Institutes of Health, National Institute of Neurological Disorders and Stroke Grants NS-34716, NS-32306, and NS-41921 and National Institute of General Medical Sciences Grant GM 25877 to P. J. Soja.


9

Can We Learn Something on Ionic Channel at the Molecular Level that Can Be Transposed to Build Technological Devices? C. Boiteux, S. Kraszewski, C. Girardet, C. Ramseyer Laboratoire de Physique Moléculaire - UMR CNRS 6624 Faculté des Sciences, Université de Franche-Comté, 25030 Besançon Cedex, France ABSTRACT

Although the presence of the membrane helps cells to retain vital ingredients, ion permeation is crucial for a variety of biological functions such as nervous signal transmission and osmotic regulation. Ion channels are proteins inserted in the membrane lipid bilayer that form aqueous pores. They are extraordinary machines acting at the nano-meter scale that allow ions to cross the hydrophobic barrier of the core membrane, guarantying to the cell a controlled exchange of ionized particles. As all membrane proteins, ionic channels are difficult to crystallize and up to 1995, no high resolution structure of a potassium channel was available. The crystallization of the KcsA and the determination of its structure by X-ray diffraction have allowed an unprecedented investigation of diffusion channels using theoretical calculations based on microscopic description of the interactions inside the protein [1]. In this communication, it will be shown how Molecular Dynamics simulation [2], and ab initio calculations [3] can explain the permeation, the selectivity between ions, the diffusion, and more recently the gating of KcsA channel [4]. As a consequence, I will show how nanosensors and nanofiltration devices based on carbon nanotubes technology can be build using our current knowledge on ionic channels. Finally, perspectives on cyto-toxocity effects of carbon nanotubes and drug vectors applications will be presented briefly.

[1] Y. Zhou, J.H. Morais-Cabral, A. Kaufman and R. MacKinnon, Nature 2001, 414, 43-48. [2] M. Compoint, P. Carloni, C. Ramseyer and C. Girardet, Biochimica et Biophysica Acta 2004, 1661, 26-39. [3] P. Huetz, C. Boiteux, M. Compoint, C. Ramseyer and C. Girardet, J. Chem. Phys. 2006, 124, 44703. [4] M. Compoint, F. Picaud, C. Ramseyer and C. Girardet, J. Chem. Phys. 2005, 122, 45427.


ORAL PRESENTATIONS


13

High Frequency Stimulation of the Periaqueductal Gray Matter & Ventromedial Hypothalamus: Amplitude and Frequency Modulation and Regional Brain c-Fos Activation Lim Lee Wei Department of Neuroscience, Maastricht University, Universiteitssingel 50 (Box 38), 6229ER, Maastricht, The Netherlands ABSTRACT

Electrical stimulation of the dorsolateral periaqueductal gray (dlPAG) and ventromedial hypothalamus (VMH) has been implicated to induce the escape or “panic-like” behavior. It remains unknown which stimulation parameters are responsible for this behavior, and also whether this can be inhibited by high-frequency stimulation (HFS). For instance, HFS has been considered very effective treatment in certain brain disorder diseases and is thought to inhibit the target structure. Relying on the “inhibitory effect” of HFS, we hypothesized that escape behavior would be inhibited by HFS when the dlPAG or VMH was stimulated. The present study examined the different frequency and amplitude response in the dlPAG & VMH microelectrode implanted male albino-Wistar rats. All animals were subjected to the stimulation parameters at: pulse width (0.1ms), frequency (1- 300Hz) and amplitude (1- 650microampere). Our results showed that HFS (90-300Hz) of the dlPAG & VMH has no inhibitory effect to the escape behavior; instead, the escape behavior was intensified in term of face validity. On the subsequent day, all stimulated animals decreased their mobility and exploratory behavior when they were introduced again into the same open-field arena. The escape threshold of stimulation was augmented when the animals were stimulated without any sufficient resting period. In addition, c-Fos activation was significantly found in the prefrontal cortex, amygdala, limbic, thalamic and hypothalamic structures of the stimulated animals. It was not possible to inhibit the escape behavior with HFS in both the dlPAG and VMH, suggesting that these structures compose of special neuroanatomical properties and require further investigation on its neurophysiological function during the modulation of electrical stimulation.


14

Expression of Recombinant Mouse Estrogen Receptor(ER) β-ligand Binding Domain (LBD) and Its Interaction with Nuclear Proteins of Mouse Brain Paramanik Vijay and Thakur MK Biochemistry and Molecular Biology Laboratory, Centre for Advanced Study, Department of Zoology, Banaras Hindu University, Varanasi -221005, INDIA ABSTRACT

Estrogen exerts multiple effects on the brain. It plays an important role in depression, mood, learning, memory, intelligence, neurogenesis and neuroprotection. Deprivation of estrogen as a result of menopause enhances degenerative changes caused by oxidative stress, and reduces the ability of brain to maintain synaptic connectivity and cholinergic integrity leading to the cognitive decline seen in aged and disease-afflicted individuals. In addition, estrogen deprivation exposes the brain to several insults like Alzheimer’s disease (AD), Parkinson’s disease, osteoporosis, cardiovascular disease and dementia. Women appear to be at an increased risk for AD and other neurodegenerative diseases due to decline of estrogen at menopause. Estrogen replacement therapy (ERT) at menopause may decrease the risk of neurodegenerative diseases, but there is a fear of developing cancer in breast and uterus. The estrogen action is mediated through two well characterized estrogen receptors (ER) α and ERβ. Like other members of the nuclear receptor superfamily, ER has three functional domains – N terminal transactivation domain (TAD) containing activation function (AF)-1, DNA binding domain (DBD) and C terminal ligand binding domain (LBD) containing AF-2. After binding to ER, estrogen induces conformational changes in the receptor, which are accompanied by the dissociation of accessory proteins like heat shock protein 90 (hsp90), thereby exposing DBD which binds to estrogen responsive element (ERE) to regulate the transcription of specific gene(s). Estrogen responsive gene regulation is dependent not only on transcription factor activation and chromatin remodeling but also on a host of coregulators- coactivators and corepressors - which bind to TAD, LBD or both simultaneously. ER acts through LBD in response to estrogen, its agonist or antagonist. Then it recruits coregulators which make a bridge between the receptor, basal transcription machinery and transcription factors resulting in differential gene expression. As the brain is exposed to declining level of estrogen with the growing age, it may be interesting to study the role of coregulators during aging of mouse brain. Here our strategy is to study the interaction of LBD with the nuclear proteins of mouse brain of both sexes. Briefly, the mouse ERβ LBD has been subcloned in a prokaryotic expression vector pRSETA followed by transformation into BL21 (DE3) competent cells. Then the mouse ERβ LBD has been expressed as His tag protein by induction with isopropyl -β-D thiogalactoside (IPTG). The expression has been found maximum at 5h after induction with IPTG at 32°C. Subsequently, the mouse ERβ-LBD has been detected by western blot analysis and purified by nickel affinity column chromatography as 22kDa and its dimer. Moreover, purified mouse ERβ LBD will be used for pull down assay to study its interaction with the nuclear proteins from male and female old mouse brain. The present study will lead to the identification of coregulators and elucidation of their function in the mouse brain with advancing age and under estrogen hormone condition. It will be helpful to understand the role of coregulators in estrogen action during neurological disorders and dementia in old age. This may also be useful in developing selective ER modulators with mixed agonist-antagonist activity functioning, e.g., agonistic in brain, bone, heart, etc. but antagonistic in breast and uterus. Keywords Coregulators, isopropyl -β-D thiogalactoside (IPTG), estrogen receptor (ER), estrogen replacement therapy (ERT), neurodegenerative diseases, pull down assay


15

Effect of CF1 on Object Recognition and Spatial Navigation In Rat Wipawee Boongvang1, Jintanaporn Wattanathorn2, Supaporn Muchimapura2, Siriporn Tiamkao3 , Chuleratana Banchonglikitkul4 and Taweesak Suntorntanasas4

1Department of Physiology and Graduate School and Neuroscience Program, 2Department of Physiology, Faculty of Medicine, Khon Kaen University, Thailand 40002, 3Department of Pharmacology, Faculty of Medicine, Khon Kaen University, Thailand 40002, 4Thailand Institute of Scientific and Technological Research, Phatumthani

ABSTRACT

In recent years, there has been a phenomenal rise in the interest of the scientific community to explore the pharmacological actions or to confirm the reputed effect of many natural products commonly used in traditional medicine. It has previously believed that eating swine’s brain could promote longevity, increase wisdom and anti-aging. Unfortunately, supported scientific document is still limited. Therefore, the current study is carried out to determine the effect of CF1, a cytoplasmic factor of swine’s brain extract, on working memory both on object recognition memory and on spatial memory. Group of adult male Wistar rats (n=8) were orally administered CF1 at doses of 0.5, 2.5 mg/kg BW once daily for 4 weeks and the animals were determined the object recognition and spatial memory using object recognition and Morris water maze tests respectively within 30 minutes after the substance administration according to the following schedule; after single dose, 1,2,3 and 4 weeks of treatment. The result showed that the CF1 at dosage used in this study induced a significant decrease in acquisition time in Morris water maze test whereas increase in exploration time in object recognition test. Therefore, it is concluded that CF1 possesses the cognitive enhancing effect and may serve as a potential nootropic agent. However, further researches are necessary in order to understand the underlying mechanism. Acknowledgement This study was supported in part by Graduate School, Khon Kaen University and Thailand Institute of Scientific and Technological Research, Phatumthani


16

Screening Effect of Zingiber Officinale Extract on Cognitive Function in Male Rats Jinatta Jittiwat1, Jintanaporn Wattanathorn2, Terdthai Tong-un2, Supaporn Muchimapura2 and Kornkanok Ingkaninan3

1Department of Physiology and Graduate School, and 2Department of Physiology, Faculty of Medicine, Khon Kaen University, Thailand 40002, 3Department of Pharmaceutical Chemistry and Pharmacognosy, Faculty of Pharmaceutical Sciences, Naresuan University, Thailand 65000. ABSTRACT

Zingiber officinale, a plant in family of Zingiberaceae. Recently, abundant of commercial products containing ginger has claimed for the cognitive enhancing effect. Unfortunately, supported document is less available. Therefore, the present study is carried out to determine the effect of this plant extract in young adult male rats. All rats were orally given the plant extract at dose 200 mg/kg BW, a dose that produced anxiolytic effect, once daily for 1 week. The animals were determined cognitive function within 30 minutes after the extract administration following single dose and 1 week of treatment using Morris water maze and object recognition test. However, no significant changes were observed. Thus, the present results do not support the cognitive enhancing effect of Zingiber officinale. However, further studies about the effect of other doses and time window of treatment are still essential. Acknowledgement This study was supported by Graduate School, Khon Kaen University and Department of Pharmaceutical Chemistry and Pharmacognosy, Faculty of Pharmaceutical Sciences, Naresuan University.


17

Neuroprotective Effect of Bacopa monnieri in Various Brain Areas. Nongnut Uabundit1, Jintanaporn Wattanathorn2, Supaporn Muchimapura2 and Kornkanok Ingkaninan3

1Department of Physiology and Graduate School and Neuroscience Program, 2Department of Physiology, Faculty of Medicine, Khon Kaen University, Thailand 40002, 3Department of Pharmaceutical Chemistry and Pharmacognosy, Faculty of Pharmaceutical Sciences, Naresuan University, Thailand. ABSTRACT

Recently, it has been found that the brain has high risk to decrease its ability due to the neuronal degeneration induced by many precipitating factors in daily life such as advancing age and emotional stress. Thus, the search for novel drugs possessing neuroprotective activity has been focused. In the present study, the effect of Bacopa monnieri, a medicinal plant possessing antioxidant and nootropic activities, was investigated. Rats were orally given the plant extract at various doses ranging from 20, 40 and 80 mg/kg BW once daily for 2 weeks and then they were determined the neuroprotective effect using the density of neurons and cholinergic neurons in various areas of hippocampus and cerebral cortex as indices. The results showed that the plant extract significantly increased the density of neurons in cerebral cortex and hippocampus. In addition, it also increased the density of cholinergic neurons in hippocampus. Therefore, our findings suggested the potential of this plant extract as neuroprotective agent and may provide advantage to protect against neurodegeneration in various neuropsychological disorders. Acknowledgement This study is supported by the National Thailand Research Council.


18

Effects of Semi-Chronic Ethanol Consumption on the Cerebellar Dentate Nucleus: A Quantitative Study in the Rats Wang T.C. and Kotchabhakdi N.

Neuro-Behavioral Biology Center, Institute of Science and Technology for Research and Development, Mahidol University, Salaya, Nakornpathom 73170 Thailand. ABSTRACT

Alcohol is widely used socially and alcohol intoxication creates important public health and social problems, including drunk-driving and automobile accidents, violent and unjustified behaviors. Chronic alcohol abuse was found to lead to permanent neurological damages of many brain areas and subsequent intellectual and behavioral impairments. Cerebellum, for instant, is well known to develop in-coordination of movements, cerebellar ataxia, loss of precision of movements and equilibrium, which produced by the damaged of alcoholism. In this work, we focus on the effects of semi-chronic alcohol consumption on the population of neurons in the cerebellar dentate nucleus which provide a major output of the cerebellum for the control of precision of skilled movements. Thirty adult male Sprague-Dawley rats weighted between 250 to 300 gm fed with fixed volume of balanced nutritional liquid diets containing six different concentrations of alcohol (0%, 5 %, 10%, 15%, 20%, and 25%) for three weeks. The rats were then anesthetized and perfused intra-cardiac with 4% paraformaldehyde fixative in Phosphate Buffer Solution. The cerebellum was removed and sectioned in coronal plane and stained with the Nissl method. The cerebellar dentate in each sections were photographed by digital microscope camera and stored for further analysis with an imaging system. The large and small neurons were digitally counted in serial sections and relative densities of the two populations of neurons of the dentate nucleus were calculated and used in order to compare the effects of different concentrations of alcohol with the control group feeding with no alcohol. There were dose-dependent significant decreases in the densities of neurons in both large and small cell populations in the dentate nucleus of rats fed with ethanol for three weeks. Therefore, we can conclude that semi-chronic alcohol consumption in adult rats (8 weeks old and up) can cause dose-dependent damages, death and loss of neurons in the cerebellar dentate nucleus. These effects may be due to either direct effects of alcohol on these populations of neurons or indirectly through the removal of inhibition by the effects of alcohol on GABAergic receptors leading to excessive excitotoxicity.


19

Differential Circadian Regulation of Clock Genes in the Hamster Pineal Gland Wongchitrat, P

2, Simonneaux, V

1, Felder-Schmidt, MP

1, Pévet, P

1, Govitrapong, P

3 and Phansuwan-Pujito, P

2

1Institute for Cellular and Integrative Neurosciences, University of Louis Pasteur,

Strasbourg, France, 2Department of Anatomy and Neuroscience Research Center,

Faculty of Medicine, Srinakharinwirot University, Bangkok, Thailand, 3Center for

Neuroscience and Department of Pharmacology, Faculty of Science, Mahidol University, Bangkok, Thailand. ABSTRACT

The pineal gland produces rhythmic secretion of melatonin under the control of the circadian clock located in the suprachiasmatic nucleus (SCN). Interestingly it has been reported recently that the rat and mice pineal gland, alike the SCN, expresses a number of clock genes. The pineal clock elements however are not involved in the daily rhythm of melatonin synthesis and their role in pineal physiology is therefore still unknown. Using a classic seasonal animal model, the Syrian hamster, we sought for the expression and regulation of several clock genes (Per1, Cry2, Bmal1, and Reverb α, analysed by in situ hybridization.) under different lighting conditions and following adrenergic treatment. Experimental groups of adult female Syrian hamsters were as follows: 1- animals kept in LD 14h:10h since birth; 2- animals kept in constant dim red light (DD) for 2 days; 3- animals kept in constant light for 2 days; 4- animals receiving adrenergic agonists at midday ; and 5- animals receiving adrenergic antagonist at night onset. We found that Per1 and Cry2 genes were similarly regulated by the circadian clock-driven norepinephrine: Per1 and Cry2 mRNA displayed a nocturnal increase maintained in DD conditions and abolished under LL conditions or after an early night administration of adrenergic antagonists. By contrast, Bmal1 and Reverb α expression exhibited a different pattern of expression and regulation. mRNA of both clock genes displayed a marked daily variation, maintained in DD conditions, with higher values at midday for Bmal1 and at day/night transition for Reverb α . Surprisingly this daily variation of both Bmal1 and Reverb α mRNA was maintained in LL conditions and was not affected by adrenergic agonists. This study confirms the daily regulation of Per1 and Cry2 gene expression by the norepinephrine in another rodent model and shows for the first time that a second set of clock genes, Bmal1 and Reverb α, are expressed with a circadian rhythm independently of the SCN-driven noradrenergic signal. This study was supported by the Royal Golden Jubilee Ph.D. Program and Cultural and Cooperation service, French Embassy in Thailand.


POSTER PRESENTATIONS


23

Possible GABAergic Modulatory Effect of Allopregnanolone in Sleep Deprivation–Induced Anxiety like Behavior and Oxidative Damage in Mice Anant Singh and Anil Kumar Department of Pharmacology, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh-160014, India ABSTRACT

Sleep is critical for maintaining physical, mental, and emotional health. Sleep deprivation or poor quality of sleep is a kind of stress, affects majority of population worldwide. Stress has been postulated to be involved in the etiopathogenesis of a diverse variety of diseases, ranging from psychiatric disorders such as depression and anxiety, immunosuppression, endocrine disorders including diabetes mellitus, male sexual dysfunction, cognitive dysfunctions, peptic ulcer, hypertension and ulcerative colitis etc. Stress increases plasma and brain levels of the neurosteroids which can have potent effects on GABAA receptors in the nervous system. In the present study, we investigated the possible involvement of GABAergic modulation in the protective effect of allopregnanolone against sleep deprivation induced anxiety like behavior and oxidative damage in mice. Pretreatment with allopregnanolone (10mg/kg and 20mg/kg ip) significantly improved locomotor activity, weight loss and anxiety. Biochemically, allopregnanolone treatment significantly restored depleted reduced glutathione, catalase activity, reversed raised lipid peroxidation and nitrite level as compared to control (72hr sleep-deprived) animals. (P<0.05). Combination of allopregnanolone (10mg/kg) with flumazenil (0.5 mg/kg) and or picrotoxin (0.5 mg/kg) decreased locomotor activity, increased anxiety, weight loss and caused oxidative damage. Combination of allopregnanolone (10mg/kg) with muscimol (0.05mg/kg) and or picrotoxin (0.5mg/kg) improved locomotor activity, weight loss, anxiety and oxidative damage. These effects were significant as compared to allopregnanolone (10mg/kg) .Flumazenil (0.5 mg/kg) and or picrotoxin (0.5 mg/kg) pretreatment blockade the protective role of allopregnanolone (10 mg/kg). However muscimol (0.05mg/kg) potentiate the protective effect of allopregnanolone. Present study indicates that allopregnanolone modulates its protective effect through GABAergic modulation. Therefore study suggests that these agents can be used in the management of sleep deprivation-induced anxiety like behavior and related oxidative damage. Keywords Anxiety, locomotor activity, oxidative stress, sleep deprivation, allopregnanolone


24

Effect of Paraoxon on GABA Uptake by Rat Hippocampal Synaptosomes Fereshteh Poorabdolhossein, Asghar Qasemi, Ameneh Shahrokhi, Ali Khoshbaten and Alireza Asgari Department of Physiology, Tarbiat Modares University, Tehran 14115-111, Iran ABSTRACT

Acute toxicity of organophosphates is the result of their irreversible binding with acetylcholinesterases, which elevates acetylcholine level. Improper handling of these agants causes poisoning characterized by convulsive seizures which may sometimes lead to death. Parathion is an organophosphate (OP) used as an agricultural insecticide.Paraoxon, an active metabolite of parathion, has been observed to be responsible for more cases of poisoning than any other (OP) insecticide. In addition to Op's anticholinesterase effects, interfere with different neurotransmitter system, specifically GABAergic pathways, termed a non-cholinergic effect of Organophosphate are progressively attracting more and more attention. In an attempt to find out the possible direct effects of paraoxon on GABAergic transmission, as potentially an undertying mechanism in Ops seizure, synatosomes originating from rat hippocampi were prepared and used. To investigate the direct modulation of GABA uptake by paraoxon. Synaptosome incubated with [3H] GABA in presence and absence of different doses of paraoxon for 10 minute in 37ºC. Finally, radioactive samples were measured by β-counter, representing the amount of GABA uptake. Our finding revealed that paraoxon at 0.01, 0.1, 1, 10, 100 μM concentrations attenuated the inhibition of GABA uptake by about: 21, 42, 27, 20, 8 % representing as compared to the data obtained from the control group. It is conclude that paraoxon can potentially interfere with GABA transporter's functions. Further investigations to elaborate more on the type of GATs involved and other mechanisms is suggested. Keywords Paraoxon, superfusion, synaptosome, hippocapmpus, GABA


25

Protective Effect of Zolpidem in Acute Immobilization Stress–Induced Certain Behavior and Biochemical Alterations in Mice and Its Possible GABAergic Mechanism Richa Goyal and Kumar Anil

Department of Pharmacology, UIPS, Panjab University, Chandigarh, India

ABSTRACT

Stress has been postulated to be involved in the etiopathogenesis of a diverse variety of diseases, ranging from psychiatric disorders such as depression and anxiety, immunosuppression, endocrine disorders including diabetes mellitus, male sexual dysfunction, cognitive dysfunctions, peptic ulcer, hypertension and ulcerative colitis. In present study, we investigated the possible involvement of GABAergic mechanism in the protective effect of zolpidem against acute immobilisation-induced behavioral modification and biochemical alterations in mice. Mice were subjected to immobilisation for a period of 6 hrs. Acute immobilisation stress for 6 hrs caused significant impairment in locomotor activity, anxiety-like behavior and antinocieptive effect in mice. Biochemical analysis revealed a significant increased malondialdehyde, nitrite activity and depleted reduced glutathione and catalase activity. Pretreatment with zolpidem (5 and 10 mg/kg, ip) significantly improved locomotor activity, anti-anxiety effect, reduced tail flick latency and attenuated oxidative damage as compared significantly to control (immobilised mice) (P<0.05). Further, Protective effect of zolpidem (5 mg/kg) was further blocked significantly by picrotoxin (1.0 mg/kg) and or flumazenil (2 mg/kg) and potentiated by muscimol (0.05 mg/kg) in immobilized animals (P<0.05). These effects were significant as compared to their effects per se. These results indicated that protective effect of zolpidem may be linked to the GABAA receptor and mediated through the benzodiazepine site, the picrotoxin site on the GABAA receptor.


26

Spinal Cord Injury Induced Oxidative Stress: Role of 3-Aminobenzamide Sankar Venkatachalam, Vijaya Prakash, Krishnan Muthaiah, Tamilselvi Palaniappan and Sridhar Skylab Department of Anatomy, Dr.ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai-600113, Tamilnadu, India ABSTRACT

The spinal cord is vulnerable to oxidative stress following the trauma. Oxidative stress refers to the imbalance between the cellular production of reactive oxygen species (ROS) and the antioxidant mechanisms that remove them (Halliwell, 1992). In terms of spinal cord injury, Oxidative stress is one of the necrotic initiating insults. Several antioxidant mechanisms serve to counterbalance the potential deleterious effects of ROS. Among enzymatic scavengers of ROS are superoxide dismutase (SOD), catalase and glutathione peroxidase (GPX) (Halliwell, 1991 and Brigelius-Flohe, 1999). The effect of 3-Ab on the enzymic and non enzymic antioxidant status in trauma induced oxidative stress is being studied. Since ROS level influences the synaptic plasticity which is well established by previous studies, ameliorating the deteriorating effect of ROS by 3 aminobenzamide enhances the potentitation in spinal circuits and it helps in synaptic reorganization of the spared circuits. Though activity dependent synaptic plasticity enhances the recovery in chronic phase, recovery should be initiated from acute phase of injury itself by counteracting the therapeutic molecular target involved in synaptic plasticity which modulated locomotor recovery.


27

Role of Oxidative Stress in Mitochondrial Dysfunctions and Behavioral Alterations in Rat Following Chronic Carbofuran Exposure Sukhdev Singh Kamboj, Vikas Kumar, Amit Kamboj and Rajat Sandhir Department of Biochemistry, Basic Medical Science Building, Panjab University, Chandigarh-160014, India ABSTRACT

Changes in neurochemical parameters, behavioral and memory performances due to carbofuran (a carbamate pesticide) treatment were investigated after chronic oral administration in rats. Carbofuran was administered to rats at a dose of 1mg/kg orally for a period of 28 days. There was a marked decrease in the activity of acetylcholinesterase (66.6%) in cerebral cortex after 28 day of carbofuran exposure. Mitochondrial respiratory chain functions were assessed in terms of MTT reduction and succinate dehydrogenase activity in isolated mitochondria. It was observed that chronic carbofuran significantly inhibited MTT reduction (31%) and succinate dehydrogenase activity (57%) in carbofuran exposed animals. This was accompanied by increase in mitochondrial lipid peroxidation (43.7%) and decrease in glutathione (66.6%) and total thiol (37.4%) content. The changes in mitochondrial oxidative stress and functions were associated with impaired cognitive functions in the animals. Diminished motor and exploratory activities and decreased performance of animals in the active avoidance task were observed. Based on these results, it is clear that carbofuran exerts its neurotoxicity by increase in the mitochondrial oxidative stress leading to mitochondrial dysfunction, which is eventually responsible for its neurotoxic effects.


28

Protective Effect of Carvedilol on 3-Nitropropionic Acid Induced Behavioral Alterations and Oxidative Stress in Rats Puneet Kumar, Padi SSV, Naidu PS and Kumar Anil Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh-160014, India ABSTRACT

3-nitropropionic acid (3-NP) is known to induce cellular energy deficit and oxidative stress related neurotoxicity via an irreversible inhibition of the mitochondrial enzyme succinate dehydrogenase (SDH). Systemic administration of 3-NP causes motor and cognitive deficits those are associated with excessive free radical generation. Recently, carvedilol has been implicated as a neuroprotectant in the treatment of various neurological disorders. The present study was designed to investigate effects of carvedilol, in 3-NP-induced cognitive impairment and oxidative stress in rats. Intraperitoneal administration of 3-NP (20 mg/kg for 4 days) showed loss in body weight, declined motor function (locomotor activity, movement pattern and vacuous chewing movements) and poor retention of memory in Morris water maze and elevated plus-maze task paradigms. Chronic treatment with carvedilol (1 and 2 mg/kg, p.o.) once daily for a period of 8 days beginning 4 days prior to 3-NP administration significantly reverse the 3-NP-induced motor and cognitive impairment. Biochemical analysis revealed that systemic 3-NP-administration significantly increase lipid peroxidation, nitrite levels, and depleted reduced glutathione levels and reduced succinate dehydrogenase activity in rat brain. Where as administration of carvedilol significantly attenuated 3-NP induced oxidative stress. It also significantly restored the decreased succinate dehydrogenase activity. The results of the present study clearly indicate that carvedilol by its antioxidant activity showed neuroprotection against 3-NP-induced motor and cognitive impairment and associated oxidative stress.


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Protective Effect of Minocycline, A Semi-Synthetic Second-Generation Tetracycline against 3-Nitropropionic Acid -Induced Neurotoxicity Manuj Ahujaª, Mahendra Bishnoi b and Kanwaljit Chopraª ªPharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh-160014, India bCentre with Potential for Excellence in Biomedical Sciences (CPEBS), Panjab University, Chandigarh-160014, India ABSTRACT

3-Nitropropionic acid is an irreversible inhibitor of the electron transport enzyme succinate dehydrogenase, a mitochondrial Complex II enzyme. Minocycline is a semi-synthetic second-generation tetracycline with neuroprotective activity and has the capability to effectively cross the blood-brain barrier. We investigated the effects of minocycline on behavioral, biochemical, inflammation related and neurochemical alterations induced by the sub-chronic administration of 3-nitropropionic acid to rats. Chronic pre-administration of minocycline (50 and 100 mg/kg) dose dependently prevented 3-NP-induced dysfunction behavioural (hypoactivity, memory retention, locomotor and rota-rod activity). In addition, 3-NP produced a marked increase in lipid peroxidation and brain nitrite levels whereas decreased the activities of catalase and succinate dehydrogenase. In contrast, pretreatment of 3-NP injected rats with minocycline resulted in the attenuation of all these alterations. A marked increase in an inflammatory cytokine TNF-α by 3-NP was also decreased by minocycline treatment. Neurochemically, the administration of 3NP significantly decreased the levels of catecholamines in the brain homogenates (dopamine, norepinephrine and serotonin) which were reversed by pretreatment of minocycline. The present finding explains the neuroprotective effect of minocycline against 3-NP toxicity by virtue of its antioxidant and anti-inflammatory activity.


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Effect of Electrical Lesion of Amygdala Basolateral-Lateral Nuclei on the Piriform Cortex Kindled Seizures in Rats P Shahabi1, SJ Mirnajafi-Zadeh1, Y Fathollahi1, N Hosseinmardi1, ME Rezvani1, A Eslamifar2 and Z Deljou2

1Department of Physiology, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran 2Pasteur Institute, Tehran, Iran ABSTRACT

Amygdala and piriform cortex have critical role in temporal lobe seizures and determination of their precise role in these kinds of seizures is very important. In this study the effect of electrical lesion of amygdale basolaterallateral nuclei on the piriform cortex kindled seizures was investigated. Rats were kindled by daily electrical stimulation of piriform cortex. In the first experiment fully kindled animals received intra-amygdala 2% lidocaine (for reversal neuronal inhibition) bilaterally. Five min later, animals were stimulated and seizure parameters were measured. In second experiment, the amygdala of kindled animals was lesioned by electrical DC current bilaterally and animals were stimulated 24 h later. Daily stimulations of these animals continued for 5 days after lesion. Intra-amygdala lidocaine reduced the kindled seizures severity. There were significant increase in stage 4 latency and decrease in stage 5 duration. Amygdala lesion reduced the seizures severity more dramatically and all seizure parameters with except to seizure stage were reduced significantly. The significant reduction in seizure parameters was observed for 4 days after amygdala lesion. The basolateral-lateral amygdala neuronal activity has a critical role in propagation of epileptic seizures from piriform cortex. Elimination of this activity decreases the severity of piriform cortex kindled seizures. However, this decrease is temporally and several days later (probably because of other brain regions activation) the seizure parameters return to their control values. Keywords Seizure, piriform cortex, amygdala, electrical lesion, lidocaine


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Involvement of Adenosinergic Receptors in Mediating the Anti-Epileptic Action of Rofecoxib (A Selective COX-2 Inhibitor) in Mice Kiran Kumar Akula, Ashish Dhir and S.K.Kulkarni University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh-160014, India ABSTRACT

Multiple lines of investigations have explored the role of cyclooxygenases (COX) in epilepsy and related CNS disorders. Cyclooxygenase particularly, COX-2 mRNA expression was found to increase in brain during seizure paradigm. In a recent study, we have elucidated the anticonvulsant action of rofecoxib (a selective COX-2 inhibitor) in various animal models of epilepsy; however, the exact mechanism of action is not yet clear. The present study investigated the possible involvement of adenosine receptors in mediating the anticonvulsant effect of rofecoxib against pentylenetetrazol (PTZ i.v.) seizure threshold model in mice. Minimal dose of PTZ (i.v., mg/kg) needed to induce different phases (myoclonic jerks, generalized clonus and tonic extensor) of PTZ convulsions were noted as an index of seizure threshold. Acute administration of rofecoxib (2 and 4 mg/ kg., i.p.), thirty minutes before PTZ infusion, produced an elevation of PTZ-seizure threshold for tonic extensor phase but it was ineffective for onset of myoclonic jerks and generalized clonus. Pretreatment of mice with sub-effective doses of either adenosine (25 mg/ kg., i.p.) or 2-chloroadenosine (1 or 2 mg/ kg., i.p.), a preferential A1 receptor agonist, produced synergism with sub-effective dose of rofecoxib (1 mg/ kg., i.p.). On the contrary, pretreatment with caffeine (100 or 200 mg/ kg i.p.) or theophylline (50 or 100 mg/ kg i.p.), both non-selective A1/A2 adenosine receptor antagonists reversed the anticonvulsant effects of rofecoxib (4 mg/ kg., i.p.). The results for the first time demonstrated that the anticonvulsant effects of rofecoxib in the PTZ i.v. threshold paradigm possibly involved an interaction with adenosine receptors. Keywords Rofecoxib, adenosine, 2-chloroadenosine, pentylenetetrazol, caffeine, theophylline, seizure threshold


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Role of Diet in the Therapy of Epilepsy in Traditional Persian Medicine Parinejad N. and Raza M. Department of Physiology, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran ABSTRACT

Diet plays an important role in the treatment of epilepsy in various traditional medicine systems. In traditional Iranian medicine, diet has been an important tool used by great physicians such as Avicenna (980-1037 AD) and Rhazes (860-932 AD). Avicenna believed that most illnesses arise solely from long continued errors of diet and regimen. Quality as well as the quantity of each meal was considered to be important in the management of epileptic patients. Avicenna, in his famous book “Cannon of Medicine” advised epileptic patients to divide their daily meal into three parts, one third for their lunch and two third for their dinner while Rhazes recommended three equal meals. They also believed that some kinds of food should be avoided (such as dairy products and apple) whereas the others are advised (such as meats and nuts). We conclude that diet was considered to be an important factor in the management of epileptic patients. Modern research has also shown that diet plays a significant role in the treatment of epileptic patients resistant to anticonvulsant drugs.


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Maternal Micronutrient Deficiency Modulates the Expression and Activity of Fetal Brain NMDA Receptor and Per Se Alters the Offspring Cognitive Functions Rosario JF and Patrick Gomez M Department of Biochemistry, St.Joseph’s College (Autonomous)-Affiliated to Bharathidasan University, Tiruchirappalli-620 002, Tamil Nadu, India ABSTRACT

Background: Behavioral consequences of maternal micronutrient deficiency are not wellunderstood, though epidemiological evidence suggests that some adult disorders like insulin resistance syndrome, behavioral abnormality and disease associated with it originate in fetal life. Maternal under nutrition is hypothesized to predispose the offspring to disease in adult life. The relevance of maternal macronutrient deficiency has been well studied but not that of micronutrients. Hypothesis: We hypothesize that chronic maternal dietary mineral (Cu or Zn) or vitamin E restriction modulates the expression and activity of fetal brain NMDAR (N-methyl –D-aspartate receptors) 11 β Hydroxysteroid Dehydrogenase-2 (11 β HSD-2) and free radical scavenging enzyme levels and per se individually alters the offspring’s cognitive function. Methods: Female weaning Swiss albino mice received a control diet (based on the American Institute of Nutrition AIN-93G diet) (n= 20) or a 50% vitamin E-restricted diet (n=20) or 50% zinc restricted diet (n=20) or 50% copper restricted diet (n=20) and they were provided with deionized water for 12 weeks and mated with control males. Pups born to the dams on the restricted diet were weaned on to the respective restricted diet. At the end of 20 weeks of feeding of the offspring, various behavioral function and activity in an open field of offspring was assessed by computerized training. Molecular analysis: Fetal brain samples were used for western blot and in situ hybridization analysis of NMDAR subunits, 11 β Hydroxysteroid Dehydrogenase-2, Super oxide dismutase, Glutathione per oxidase, Glutathione Reductase, Catalase in both control and micronutrient deficiency groups. Results: Body weight and crown rump length were significantly (p<0.001) reduced in offspring, from dams fed micronutrient diet compared with control group. The micro nutrient restricted (Cu or Zn or Vit E) mice had significantly increased locomotors activity. Western blot analysis and in situ analysis of 11 β HSD-2 expressions, Super oxide dismutase, Glutathione per oxidase, Glutathione Reductase, Catalase in fetal brain were down regulated in all the restricted diet fed groups. Micronutrient deficiency significantly alters the NR1 mRNA inCA1/2 and CA3 subfields of the hippocampus. Conclusion: Maternal micronutrient deficiency during conception and early life period has profound consequences on behavior and development of crucial neurotransmitter systems in postnatal life.


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Effects of Ascorbic Acid on Streptozotocin Induced Oxidative Stress and Memory Impairment in Rats Weerateerangkul, P Department of Physiology, Faculty of Medicine, Chiang Mai University, Thailand ABSTRACT

Streptozotocin (STZ) is a glutamine-nitrosourea compound that shows selective cytotoxic to pancreatic beta cells. Though the mechanisms of the induction of diabetes are not clear, it is proposed that STZ be related to the generation of free radicals which results in DNA fragmentation or protein deformation. If injected intracerebroventricularly, STZ can produce oxidative stress in the brain and memory impairment that probably cause sporadic Alzheimer's disease, one type of senile dementia which has the progressive loss of memory. Since ascorbic acid (AA) has been shown to have high antioxidant properties in many studies. The present study was undertaken to assess the potential of AA as memory-enhancer via mechanisms of reduction of free radical and increase in reduced glutathione (GSH) as free radical scavenger. The experiment was performed in male Wistar rats of about 250 g BW. The animals were divided into 2 groups: the first group as the vehicle-treated group and the second group as the STz-treated group. The STZ was injected into the lateral ventricle of the brain, 3 mg/kg BW. The animals in each group were divided into 4 groups in accordance with dose of AA treated (0, 50,100, 200 mg/kg BW). AA was injected daily for 21 days. On day 19th and 20th of AA treatment, the animals were tested for memory retention using an elevated plus-maze. After completing the experiments, the brains of all animals were collected and homogenized for further biochemical determination of malondialdehyde (MDA) and reduced glutathione (GSH). It was observed that all animals untreated with STZ were not different regarding memory retention and biochemical aspects. However, the STZ only-injected animals showed decreased memory retention as the oxidative stress increased, reflected as the increased MDA level and decreased GSH level. The beneficial effects of AA treatment were shown in animals treated with both AA and STZ that the significant recovery memory was observed in accompanying with reduced oxidative stress. The effects are seemingly in dose-dependent manner. The results of this study show that AA can be effective in decreasing oxidative stress and help recovery of damages in cognitive function caused by intracerebroventricular STZ injection.


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Regional Differences in Microglial Susceptiblity to Amyloid Beta in the Rat Brain Prabhakar Singh and Taposh Kumar Das Department of Anatomy, All India Institute of Medical Sciences, New Delhi 110029, India ABSTRACT

Alzheimer’s disease primarily affects hippocampus and associated areas responsible for memory and cognition however, other unrelated areas such as cerebellum are almost unaffected. Microglia are considered important in progression of different pathological consequences including Alzheimer’s disease. The regional difference in microglial susceptibility with lipipolysaccharide was reported earlier and hypothesized that these regional differences may contribute to localized pathogenic response. To evaluate the hypothesis we use acute intracerebroventricular injection of amyloid beta to the different regions namely frontal cortex, hippocampus and cerebellum of the rat brain. The microglial response was assessed after ten days of injection in brain cryosections. Anti-OX42 and anti-OX6 (activated microglia) antibodies were used for immunohistochemical localization of microglia. In this study we found that microglial density is comparatively high in hippocampus region compared with frontal cortex and cerebellum. Region-specific differential susceptibility to amyloid beta is attributable to differences in the number of microglia present within the region and may reflect levels of inflammatory factors produced by these cells.


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Protective Effects of N-(2-Propylentanoyl) Urea on CA1 and CA3 Neuronal Cell Death after Common Carotid Arteries Occlusion in Mice Oraphan Wanakhachornkrai1, Boonyong Tantisira2 and Mayuree H. Tantisira2 1Inter-department of Physiology, Graduate School, Chulalong korn University, Bangkok, Thailand 2Research Unit of Neurophysiology and Neuropharmacology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok 10330, Thailand ABSTRACT

The present study aimed to investigate the effects of N-(2-propylpentanoyl) urea (VPU) on impairment of learning and memory and CA1 and CA3 neuronal cell death after transient cerebral ischemia (bilateral occlusion of common carotid arteries, 2VO) in mice. The 2VO caused a reduction in latency and an increase in number of errors in passive avoidance (step-down) test. Accordingly, increases in brain malondialdehyde (MDA) as well as neuronal cell death in hippocampus CA1 and CA3 regions were also observed. Intraperitoneal administration (i.p.) of VPU significantly increased the step-down latency and decreased the number of errors in this task. In addition, an increase in MDA induced by 2VO was completely abolished. Number of survival neurons in CA1 and CA3 regions of hippocampus in VPU-treated mice was significantly higher than those observed in 2VO group. Improvement in the step-down test is likely to be explained by protection of neuronal cell death as well as anti-oxidative effects observed. Multi-mechanisms of VPU previously reported e.g. potentiation of GABA, inhibition of NMDA receptor and a reduction of cortical glutamate might underlie the neuroprotective effect observed in the present studies.


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Screening of Indian Herbal Medicine in the Treatment of Alzheimer's Disease P. Levin Michel Anbu Gomez Department of Biotechnology, Annamalai University, Chidambaram, Tamilnadu, India ABSTRACT

Alzheimer's disease (AD) is characterized by profound memory loss sufficient to interfere with social and occupational functioning. It is the most common form of dementia, affecting more than 20 million people worldwide. AD is characterized by an insidious loss of memory, associated functional decline, and behavioral disturbances. Patients may live for more than a decade after they are diagnosed with AD, making it the leading cause of disability in the elderly. The incidence of AD ranges from 1 to 4 percent of the population per year, rising from its lowest level at ages 65 to 70 years to rates that may approach 6 percent for those over the age of 85 years. The first neurotransmitter defect discovered in AD involved acetylcholine (ACh). As cholinergic function is required for short-term memory, the cholinergic deficit in AD was also believed to be responsible for much of the short-term memory deficit. Clinical drug trials in patients with AD have focused on drugs that augment levels of ACh in the brain to compensate for the loss of cholinergic function. These drugs have included ACh precursors, muscarinic agonists, nicotinic agonists, and acetylcholinesterase inhibitors. The most highly developed and successful approaches to date have employed acetylcholinestrase inhibition. Although some Food and Drug Administration-approved drugs are available for the treatment of Alzheimer's disease, the outcomes are often unsatisfactory, and there is a place for alternative medicine, in particular, herbal medicine. Our interest is to screen the medicinal plants for the in vivo and in vitro activities against AD. Here I am presenting the clinical effects of a number of commonly used types of herbal medicines for the treatment of AD.


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Effects of Thai Traditional Herbal Formulas (Yahom) on the Central Nervous System Aree Wanasuntronwong1, Boonyong Tantisira2 and Mayuree H. Tantisira2

1Inter-department of Physiology, Graduate School, Chulalongkorn University, Bangkok, Thailand 2Research Unit of Neurophysiology and Neuropharmacology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok 10330, Thailand ABSTRACT

Locomotor activity test and Barbiturate Potentiation test were used to investigate the effects on the central nervous system (CNS) of three extracts of Thai traditional herbal formulas commonly used to relieve vertigo, namely, Yahom Navagote (YN), Yahom Prasatthong (YP) and Yahom Intajak (YI) in mice. Solution of 5% Tween 20 in distilled water was used as a vehicle for the preparation of test substance given to the experimental animals by gavage tube. YP and YI in the doses of 300, 1000 and 3000 mg/kg B.W. did not exert either significant stimulant or depressant effect on the CNS as indicated by a lack of their effect on locomotor activity when the extract was given alone. However when these two extracts were given to mice receiving pentobarbital 50 mg/kg B.W., non-dose related prolongation of sleeping time was observed. In the other hand YN in the dose of 100, 300, 1000 and 3000 mg/kg B.W. significantly depressed locomotor activity in a non-dose related manner. Further investigation by Barbiturate Potentiation test revealed a dose- related prolongation of barbiturate, however, a statistical significance was noted only at the dose of 3000 mg/kg B.W. of YN. Therefore, YN seems to exert significant depressant effect on CNS whereas YP and YI are devoid of this effect. Possible neuromuscular blockade by YN should be further ruled out and investigation of their effects on pentobarbital metabolizing enzyme, Cytochrom P 450, is warranted to clarify barbiturate potentiating effects of the test compounds.


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Effect of Persistent Pain on the Synaptic Transmission in Hippocampal Formation Ya-li Long, KE-RUI GONG, Ming-gang Liu, Zhen LI, Xiao-yan Zhao, Cui-ying Gao, Xue-feng Chen, Rui-rui Wang, Yong Xiao, Xiu-yu Cui,Hua Li,Yang-yuan An, Lan-feng Zhao and Jun Chen Institute for Biomedical Sciences of Pain, Capital Medical University, Beijing, P.R.China ABSTRACT

Pain can activate several cortex areas which include anterior cingulate cortex (ACC), the first somatosensory, insular cortex and hippocampus formation. And the plasticity of these area are suspected to take part in the maintenance of the persistent pain. Here, some preliminary data about the effect of persistent pain on the synaptic transmission in the hippocampus formation were provided. The male SD rats were divided into two groups at random. One was control group without any treatment. The other one was the persistent pain model group and in this group, the rats were given subcutaneous Bee venom (BV) injection on the hind paw. Two hours after injection of BV, the slice of the hippocampus was made. And at the according time, the slice of the control group was also made. Whole-cell recordings using the “blind” patch technique or differential interference contrast (DIC)-enhanced infrared (IR) videomicroscopy were applied to study the synaptic transmission in the hippocampus. The miniature exictory postsynaptic currents (mEPSC) and miniature inhibitory postsynaptic current (mIPSC) in CA1, CA3 and dentate gyrus (DG) were recorded and their frequency, half width and amplitude of mEPSC and mIPSC were analyzed. We found the persistent pain caused by BV s.c. injection decreased the frequency of mEPSCs in DG by 72% compared with the control group. But the pain didn’t change the amplitude and half width of the mEPSC in CA1, CA3 and DG areas. 2) As for the mIPSC, BV s.c. injection decreased its frequency in DG area by 71%, but increased its frequency by 62% in CA3 area. BV s.c injection didn’t affect the frequency of mIPSC in CA1 area. The persistent pain caused by BV injection increased the half width of mIPSC in CA1 and DG area for 66% and 55% respectively. And the pain had no effect on the half width of mIPSC in CA3 area. The amplitude of mIPSC was not affected by BV injection in CA1, CA3, and DG compared with control. This suggested that the persistent pain can change the synaptic transmission of the hippocampus, and whether the synaptic transmission in other areas such as ACC remained to be studied.


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Involvement of MAPK Pathway in the Generation and Maintenance of Bone Cancer Pain Li Tingting, Zhao Zhiqi, Ji Rurong and Zhang Yuqiu Institute of Neurobiology, Institutes of Brain Science, Fudan University, Shanghai 200032, China ABSTRACT

Activation of MAP (Mitogen-activated protein) kinase pathway in spinal dorsal horn by peripheral noxious stimulation contributes to both short-term and long -term pain hypersensitivity. Recently, we studied a rat model of bone cancer pain to investigate the possible mechanism of cancer pain. Syngeneic Walker 256 mammary gland carcinoma cells were injected into the tibia medullary cavity.Bone radiology, bone histology method, behavioral techniques, immunohistochemistry, pharmacology method and electrophysiology methods were used to study the role of MAPK pathway plays in bone cancer pain. We analyzed the extent of tumor-induced bone destruction, mechanical and hyperalgesia, and neurochemical characterization of the peripheral and central systems during bone cancer pain. From the results of radiology and histology of tibia bone, 7days after inoculation with Walker256 cell, there was no significant change with bone. 14days after inoculation, there was slight bone destruction and significant bone destruction was found 21days after inoculation, lots of trabecula of bone and periosteum were lost. Mechanical allodynia occurred about 8days after inoculation, and maintained to 21day both in ipsilateral and contralateral side. Through immunohistochemistry, we observed the expression of phosphorylation extracellular signal-regulated kinase (ERK) and p38, members of MAPK family. Phaspho-ERK (p-ERK) and phospho-p38 (p-38) were both increased in the spinal dorsal horn, 3, 7and 14days after inoculation, and p-p38 was colocalization with OX-42 which is marker of microglia. There will be a metastasis of pERK from microglia to astrocyte .These results indicate that MAPK pathway may play a role in bone cancer pain. The deeply study is going.


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Electrical Stimulation on the Denervated Muscle Attenuates Neuropathic Pain after Spared Nerve Injury Supin Chompoopong1, Kanyarat Bamrungsuk1, Kanokwan Tilokskulchai2 1Department of Anatomy and 2Department of Physiology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand ABSTRACT

The mechanisms responsible for peripheral neuropathic pain after nerve injury are not fully understood. One hypothesis is that early ectopic discharges of damaged fibers and dorsal root ganglia (DRG) and sprouting of afferent fibers produce activity-dependent irreversible changes in the central nervous system. The aim of this study was to determine whether blockade of peripheral discharge by electrical stimulation on the denervated muscle could prevent the development and persistence of neuropathic pain in the spared nerve injury model (SNI). After a spared nerve injury procedure in adult rat was performed, stimulation of the denervated muscle by low-frequency electricity (2 Hz) before and 1, 2 and 3 weeks after the injury were done. Development of neuropathic pain behavior was assessed for 5 weeks by withdrawal responses to von Frey filaments stimulation in SNI and in sham rats. The myelinated primary afferents were labeled with cholera toxin B subunit (CTB), a selective myelinated fiber tracer that identifies transganglionic synapses. And the localization of substance P (SP) immunoreactivity was examined in the dorsal horn of spinal cord and DRG. The electrical stimulation on the denervated muscle produced conduction blockade with an increase in withdrawal thresholds in the sural territory after 2 weeks. The stimulation also resulted in decrease SP immunoreactivity in the dorsal horn of spinal cord and DRG in SNI rats. These results indicate that the peripheral and spinal SP reveal an increased reactivity in a neuropathic pain model. Therefore, the peripheral disharge blockade has effect on the development of tactile allodynia after SNI. Keywords Low frequency electrical stimulation, spared nerve injury, neuropathic pain


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Cisplatin-Induced Neuropathy in the Rat Model: Differences between Genders Tulaporn Wongtawatchai, Sithiporn Agthong and Vilai Chentanez Department of Biomedical Science, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand ABSTRACT

Cisplatin (cis-diaminodichloroplatinum), is widely used as an antineoplastic agents, but causes sensory neuropathy are one of the major side effects. The sex difference affects the regeneration rate and severity in diabetic neuropathy. However, this phenomenon has not been examined in cisplatin induced neuropathy. Therefore, the aim of this study was to investigate the motor and sensory function following cisplatin injection. The hot plate test and motor nerve conduction velocity (MNCV) was examined on the hindpaw. We give cisplatin intraperitoneally 2 mg/kg twice a week for ten doses in male (MC) and female (FC) rats. The control groups were injected with NSS as a vehicle both in males (MN) and females (FN). For the general toxicity, both MC and FC showed decreasing in body weight in 1st week compare with the controls. Other aspects of general toxicity, e.g. piloerection, toe-walking, arched back was observed in the FC group earlier than in the MC group (from the 2nd week). All rats in the FC group survived until the end. In contrast, the MC group developed these abnormalities later after the 5th week with sudden loss of four rats. Concerning, the hot plate test were observed thermal hypoalgesia which significantly difference between control and cisplatin treated group in both sex in 2nd week. MNCV were decreased in FC group and MC group from 3rd and 5th week, respectively. This data suggest that gender might have an influence on the development of cisplatin induced neuropathy.


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Protective Effects of Centrophenoxine, an Antiaging and Antioxidant Drug, against Rotenone Induced Parkinson Disease Ranjeet Verma and Bimla Nehru Department of Biophysics, Panjab University, Chandigarh-160014, India ABSTRACT

Rotenone, a potent specific inhibitor of mitochondrial complex I appear to reproduce the feature of Parkinson’s disease in the rats. It destroys dopaminergic neurons selectively causing deficiency of dopamine in stratum which leads to impaired motor functions. It is proposed in present study that rotenone toxicity is mainly due to the production of reactive oxygen species and it could be prevented by the use of antioxidants. In present study SD male rats were administrated with rotenone on a daily basis by subcutaneous injection of dose: 2mg/kg body weight per day over a period of 5 weeks. Data showed impaired motor function (such as a strong increase in catalepsy, decrease in locomotor activity), significant decrease in dopamine and alteration in antioxidant defense system( decrease in GSH, Cu/Zn SOD and increase in NO, cutrulline LPO) . Present study explores the potential of centrophenoxine, a strong antioxidant and a well known anti aging drug against rotenone induced neurotoxicity. It is found that centrophenoxine is effective in attenuating all the motor dysfunction, neurochemical and biochemical alterations induced by rotenone toxicity, when given as co-treatment at a dose of 100mg/kg body weight per day intraperitoneally for a period of five weeks. Thus suggesting that centrophenoxine may be helpful in developing therapeutic strategies for Parkinson’s disease and other neurodegenerative diseases where oxidative stress is more prevalent factor.


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The Neuroprotective Effect of Melatonin and Monoamine Uptake Blocker on SH-SY5Y Dopamine Cell Line Chutikorn Nopparat1, Piyarat Govitrapong1,2, and Banthit Chetsawang1

1Neuro-Behavioural Biology Center, Institute of Science and Technology for Research and Development, Mahidol University, Salaya, Nakornpathom 73170, Thailand 2Center for Neuroscience and Department of Pharmacology, Faculty of Science, Mahidol University, Bangkok, Thailand

ABSTRACT

The degeneration of dopaminergic neurons of the substantia nigra is responsible for primary motor symptoms observed in Parkinson’s disease. It has been reported that overproduction of reactive oxygen species occurs after brain injury and mediates both necrotic and apoptotic cell death. Recently, melatonin has been reported to process an efficient antioxidant capacity. In addition, an inhibition of cell death induced by neurotoxin with a monoamine uptake blocker has been demonstrated. In the present study, the protective roles of melatonin and desipramine, a monoamine uptake blocker against neuronal cell death have been investigated in human dopaminergic neuroblastoma SH-SY5Y cultured cells. The present results demonstrated that desipramine was able to diminish the toxic effects of neurotoxin, 1-methyl-4-phenylpyridinium iodide (MPP+) but not hydrogen peroxide on cell viability reduction. However, the protective effect of melatonin on hydrogen peroxide reduced cell viability was demonstrated in SH-SY5Y cultured cells. Further study on the mechanisms of these two compounds in protecting the toxic effect of dopamine cell is necessary. Acknowledgement This work was supported by the Thailand Research Fund (RSA4780018).


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The Effects of Genistein on Okadaic Acid-Induced Hyperphosphorelated Tau Protein in SH-SY5Y Cells In Vitro Siriporn Chamniansawat and Sukumal Chongthammakun Center for Neuroscience and Department of Anatomy, Faculty of Science, Mahidol University, Bangkok 10400, Thailand ABSTRACT

Hyperphosphorylation of tau protein is a major component of neurofibrillary tangles (NFTs) seen in Alzheimer’s neurons. The tangle-containing neurons eventually die. Tau protein is a microtubule-associated protein (MAP). Normally, tau proteins interact with tubulin to stabilize microtubules and promote tubulin assembly into microtubules, whereas in Alzheimer’s neurons tau is phosphorylated at many sites leading to detach from its microtubule and self aggregate into NFTs. However, the exact causes of tau hyperphosphorylation remain unclear. The imbalance of enzyme kinase and phosphatase activity is interesting as the underlying mechanism of Alzheimer’s disease (AD). Glycogen synthase kinase-3β (GSK-3β) and protein phosphatase-1,-2A (PP-1, PP-2A) play a significant role in the regulation of phosphorylation and dephosphorylation of tau protein, respectively. Previous studies showed that estrogen decreased phosphorylated tau by inducing inactive GSK-3β. Unfortunately, the undesired side effects of estrogen such as proliferative and oncogenic effects on non-neuronal cells have been reported. In this study, we aim to investigate the possibility of using genistein as an alternative estrogenic agent for the neuroprotection by examining the effects of genistein on tau phosphorylation and inactivation of GSK-3β in SH-SY5Y cells induced by okadaic acid (OA). The expression and the location of phosphorylated proteins were detected by western blot analysis and immunocytochemistry, respectively. The results showed that genistein significantly reduced the amount of tau phosphorylation induced by OA and increased the inactive form of GSK-3β via estrogen receptor (ER) activation. These present data suggest that genistein is a potential neuroprotective agent for further utilize in therapeutic approaches to neurodegenerative diseases such as AD.


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Signaling Pathway in Methamphetamine-Induced tPA Gene Expression Kanchanat Ternchoocheep and Sukkid Yasothornsrikul Department of Biochemistry, Faculty of Medical Science, Naresaun university, Phitsanulok, Thailand ABSTRACT

Tissue plasminogen activator (tPA) is a serine protease which activate plasminogen (plg) into plasmin. It involves in neurite outgrowth and neuronal development by cleaving proteins of extracellular matrix and forming a path for extending neuronal processes. Recently it is found to associates with late phase of long-term potentiation, learning and memory, exocytotoxic neurodegeneration and recovery from neuronal injury. Thus, tPA is related to the regulation of numerous aspects of synaptic plasticity and remodeling. The tPA has been revealed its relationship with some drugs of abuse such as methamphetamine (Meth), morphine, and cocaine. Methamphetamine may regulate tPA gene expression through dopamine receptors via downstream signaling and / or CREB transcription factor. Therefore, this study is aim to investigate Methamphetamine signaling pathway that induces tPA gene expression whether it passes through dopamine receptors and CREB. The results from this study will further the understanding on basic mechanisms of methamphetamine dependence and will be beneficial in therapeutic aspects.


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Polymorphism of Glutamate N-Methyl-D-Aspartate Receptor Subunit 2B in Methamphetamine Abusers Rachanee Chanasong1, Samur Thanoi1, Paritat Watiktinkorn2 and Sutisa Nudmamud-Thanoi1

1Department of Anatomy, Faculty of Medical science, Naresuan University, Thailand. 2Central Institute of Forensic Science (CIFS), Ministry of Justice, Thailand ABSTRACT

Background: Glutamate N-methyl-D-aspartate receptor 2B (NMDAR2B) is a subunit of NMDA receptors. Polymorphism of NMDAR2B gene has been demonstrated in patients of schizophrenia, alzheimer’s disease, parkinson’s disease, and alcoholic dependence. Aims: To investigate NMDAR2B polymorphism in methamphetamine abusers and its association with symptom of dependence. Methods: The subjects in this study comprised of 50 male methamphetamine abusers, with dependent symptoms according to DSM IV criteria, and 50 controls which matched sex and age. The genotypic study of NMDAR2B was carried out by PCR from dried- blood samples collected with FTA® cards, followed by a restriction fragment length polymorphism (RFLP) analysis of the amplified products. Association of genotype frequencies and allele frequencies between subjects and controls were then analyzed using Fischer’s exact test. Results: The genotype frequency of NMDAR2B and allele frequency between controls and methamphetamine abusers were significantly different (P < 0.05); allele T presence to T absence of control groups and abusers were 0.63:0.37 and 0.58: 0.42 respectively. In details, statistical differences were also found between controls and subjects with withdrawal, excessive amount of use/ time and decrease social activity manifestations, (P < 0.05). Conclusion: The polymorphism of NMDAR2B might have been associated with methamphetamine dependence. The observed difference in T allele between control and methamphetamine dependence might play a role in genetic susceptibility to methamphetamine dependence. Further study with larger sample size, and female group are needed.


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Phosphorylation of cAMP Response Element Binding Protein Induced by Group I Metabotropic Glutamate Receptors in Astrocytes : Prelimainary Studies Kittikun Viwatpinyo and Sukumal Chongthammakun Center for Neuroscience and Department of Anatomy, Faculty of Science, Mahidol University, Bangkok, Thailand. ABSTRACT

Glutamate is known as a major excitatory neurotransmitter in the central nervous system. Beside its synaptic transmission properties, glutamate is also involved in intracellular signal transductions via metabotropic glutamate receptors (mGluRs). These signaling cascades might lead to gene regulation by activation of transcription factors. Despite of extensive studies in neurons, effects of glutamatergic signaling remain unclear in glial cells. This study is aimed to investigate the in vitro effect of glutamate on activation of transcription factor cAMP response element binding protein (CREB) in astrocytes. Cultures of 1-2 days postnatal rat cortical astrocytes were established, and subjected to glutamate at various dosage and time. The level of CREB phosphorylation at serine-133 residue was evaluated by western immunoblotting. Glutamate treatment at various time intervals reveals that phosphorylation reaches its peak within 5 minute after glutamate treatment, and then declines gradually. For the dose dependency result, the level of phosphorylated CREB is found highest around 0.1 mM and 1 mM of glutamate, but not significantly higher than control group. Moreover, experiment by pretreatment the cultures with different Ca2+ chelators shows that phosphorylation of CREB is attenuated when BAPTA-AM, an intracellular Ca2+ chelator, was applied. In conclusion, glutamate can elicit rapid, transient phosphorylation of CREB in astrocyte in vitro, and this should depend on intracellular calcium level. Proposed further investigations include the use of potent, specific group I mGluRs agonist and antagonist instead of natural ligand, and inhibition of calcium-responsive signaling molecules. Keywords Glutamate, astrocyte, cAMP response element binding protein


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Different Effects of Naloxone on Sweet Food Intake of Repeated Restraint-Stress Rat and Non-Stress Rat Suwaporn Daendee1, Sarinee Kalandakanond-Thongsong2 and Sutthasinee Poonyachoti2

1Inter-Disciplinary program of Physiology, Graduate School, Chulalongkorn University, Bangkok, Thailand 2Department of Physiology, Faculty of Veterinary Science, Chulalongkorn University, Bangkok, Thailand ABSTRACT

Involvement of opioid systems has been suggested in various stress responses. Behavioral disorders including overeating of palatable food were found in stress animals. The present study aimed to investigate the roles of the endogenous opioid system in the development of sweet food intake in rats exposed to chronic restraint stress. Male Wistar rats were divided into two groups: control (CON) and stress (ST), which rats were restraint 1 h/day, for 14 days. Both groups were subdivided into two groups; treated with or without non-selective or selective μ-, δ- or κ-OR blockers (naloxone, CTOP, naltridole, or nor-binaltorphimine dihydrochloride, 0.5-1 mg/kg. BW, S.C., 30 min before the behavioral test). In the sweet food intake test, the rats were placed in the cage and allowed to consume sweet food (Froot loops ® pellets), the number of ingested pellets during a period of 6 min was then recorded. The present study revealed that sweet food consumption was increased in chronic restraint stress rats (7.02 pellets, n= 5, p<0.005) compared to control rats (3.81 pellets, n= 5, p<0.005). Increased sweet food consumption in stress group was attenuated by subcutaneously injection of non-selective OR antagonist, naloxone (0.5 mg/kg BW, s.c), 30 min prior to the sweet food intake. Unlike stress rat, selective k-OR antagonist (nor-BNI, 1 mg/kg BW, s.c) injection increased the sweet pellet consumption. However, selective μ- (CTOP) or δ- (naltrindole) OR antagonist treatment had no effects on in this study. The evidence suggested the changes of opioid receptor system in regulating of sweet food consumption are subject in restraint stress animals. These results suggested that chronic stress causes an increase in sweet food intake, and opioid system partially regulated stress induced-sweet food intake. Although the types of specific opioid receptors responsible for sweet food intake could not be ruled out, it is suggested that μ- opioid receptor may be a candidate for this effect.


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Localization of Delta Opioid Receptors in Efferent Nerve Fibers of the Rat Cochlear

Kwankanit Saeung1, Pansiri Phansuwan-Pujito1, Stefano Casalloti2, Andrew Forge2 and Piyarat Govitrapong3

1Department of Anatomy, Faculty of Medicine, Srinakharinwirot University, Bangkok. 2Institute of Laryngology and Otology, University College London, England. 3Center for Neuroscience and Department of Pharmacology, Faculty of Science Mahidol University, Bangkok, Thailand. ABSTRACT

The presence of delta opioid receptors (DOR) has been recently demonstrated in the rat cochlea by both reverse transcriptase-polymerase chain reaction and immunohistochemistry. The DOR have been localized in the inner and outer hair cells, and bipolar cells of the spiral ganglion which were suggested to be postsynaptic type. In addition, they were also found in nerve fibers within the spiral ganglion and intraspiral bundle. These receptors may be presynaptic type on either opioidergic or non-opioidergic efferent nerve fibers. The main neurotransmitters of efferent nerve fibers were acetylcholine and GABA. In order to elucidate this, the double immunohistochemical studied has been performed in the rat cochlea using antisera against choline acetyltransferase (ChAT), a cholinergic indicator, GABA and leu-enkephalin together with an antiserum against DOR. There were some colocalization between DOR and ChAT, and DOR and leu-enkephalin within an intraganglionic bundle. A very few of DOR was found to colocalized with GABA. Moreover, double staining using antisera against DOR and synaptophysin were also done to prove the presynaptic role of DOR. The results from this study confirm that the DOR presence in the nerve fibers of the rat cochlea are presynaptic type and involve in controlling of neurotransmitter released from the efferent nerve fibers, either opioidergic or non-opioidergic efferent nerve fibers such as acetylcholine and GABA.

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