Chapter 16

Chapter 16

Neural Integration II:The Autonomic Nervous

System and Higher-Order Functions

Sensory Motor

General (15)

Special (17)

Somatic (15)

Autonomic (16)

fig. 15-1

fig. 16-1

Autonomic Nervous System (ANS)

regulate homeostasisworks independent of consciousness

Autonomic Nervous System (ANS)

compared to Somatic NS

fig. 16-2

fig. 16-3

Sympathetic

prepare body for heightened levels of somatic activity

“fight or flight” response

•increased mental alertness•increase metabolic rate•reduced digestive/urinary fn•activation of energy reserves•increase respiration rate•increase heart rate, bp•activation of sweat glands

fig. 16-7

parasympathetic

stimulates visceral activity

“rest and repose”conserve energypromote sedentary activities

•decrease metabolic rate•decrease heart rate, bp•increase secretion-digestion•more blood to digestive system•stimulate urination/defecation

sympatheticparasympatheticENS

enteric nervous system

complex visceral reflexes

sympathetic nervous system

preganglionic neurons

T1 to L2 lateral horn of spinal cord

project to ganglia (3)

sympathetic chain gangliacollateral gangliaadrenal medulla

lots of divergence (1 to many)

fig. 16-4

fig. 16-5 sympathetic nervous system

collateral ganglia

celiacstomach, liver, gall bladderpancreas and spleen

superior mesentericsmall intestineproximal 2/3’s of large intestine

inferior mesentericlarge intestine, kidneys, bladder reproductive organs

fig. 16-4b

Adrenal medulla

receives preganglionic sympathetic input

synapse on neuroendocrine cells of medulla

cells secrete E or NE into blood

epinephrinenorepinephrine

adrenalinenoradrenaline

fig. 16-4c

CRISIS

sympathetic activation

controlled by centers in the hypothalamus

increased alertness RASfeelings of energy and euphoria

(disregard for danger, insensitivity to pain)

Increase heart and lung activity(controlled by pons and medulla)

Elevation of muscle toneMobilization of energy reserves

sympathetic neurotransmitters

preganglionic neurons use ACh(cholinergic)

postganglionic neurons release NE(adrenergic)

postganglionic cells have varicositiesinstead of axon terminals

fig. 16-6


affect is longer lasting thanat a neuromuscular jn (Ach; 20 msec)

NE affects its targets until it is reabsorbed or broken down (seconds)

NE adrenal medulla lasts even longer(minutes)


Most of the NE released is reabsorbed by the neruon (50-80%) reabsorbed NE is re-used or broken down by MAO (monoamine oxidase)

the rest diffuses away and is broken down by COMT in the tissues

receptors for NE

Two classes

alpha beta

both are G-proteins(second messengers; 12)


neurotransmitters andneuromodulators

How do they work?

1. direct effect onmembrane potential

2. indirect effect onmembrane potential

3. diffusion into cell

2.

fig. 12-17

fig 12-17

alpha receptors

-1

-2

more commonrelease intracellular Ca2+

stimulates target cell

lowers cAMP levels in cell(inhibitory on target cell)found on parasympathetic cells


beta receptors

in membranes of many organsheart, lungs, liver, muscle, …


changes metabolic activity of target cells (intracellular cAMP)

beta receptors

-1

-2

increased metabolic activityskeletal musclecardiac output

inhibitoryrelax smooth m. in resp. tracteasier to breath (asthma)


beta receptors

-3

found in adipose tissuecauses lipolysisrelease fatty acids for metabolism


other transmitters


ACh

NO (nitric oxide)

sweat glands in skin (secretion)blood vessels to brain and muscle

(dilation of vessels)

vasodilation in brain and muscle

to here3/16/07lec# 27

uses sympathetic chaincollateral gangliaadrenal medulla

short preganglionic, long postgang.excessive divergence (2 doz +)pregang. cells release AChMost postgang. cells release NE

a few use ACh, NOResponse depends on receptors ()

sympathetic summary

sympathetic summary

neurotransmitters and receptors:

ACh

NE ACh NO

pre-

post-

receptors

most

common-stimulatory

inhibitory increaseskel. muscle

cardiac output

inhibitory(airways)

fat cellslipolysis

Parasympathetic nervous system

fig. 16-7


preganglionic cells in nuclei in:midbrainponsmedulla oblongataspinal cord

travel with:CN III, VII, IX, Xpelvic nerves S2 to S4

preganglionic cells:

less divergence than sym.(6-8)

postganglionic cells:in terminal ganglia (near organ)

orintramural (in organ)

effects more localized and specific


fig. 16-8

CN III

VII

IX

X

pelvic

CN III, VII, IX

control visceral structures in the head

CN X

neck, thoracic and abdominal cavities(75% of parasympathetics)


constrict pupilsclose visionstimulate digestion secretionssecretion of hormones-cellular nutrient usesexual arousal changesincrease smooth m. activity - digestive sys.stimulate/coordinate defecationcontract urinary bladder for urinationconstrict airwaysreduce heart activity

Parasympathetic activation

ACh

Parasympathetic neurotransmitters

fast actinginactivated quickly by AChE

localized effects

Receptors


two types: nicotinic

muscarinic

on ganglion cellsmost muscles (SNS)lead to epsp

parasym. muscle, glandsG proteinsepsp or ipsplonger lasting

Receptors


nicotinic

muscarinic

nicotine poisoning (50 mg):vomiting, diarrhea, high bprapid heart rate, sweating,…

nausea, vomitting, diarrhea,constriction of airways, low bplow heart rate

100 keys (pg. 530)

“The preganglionic neurons of the autonomic nervous system release acetylcholine (ACh) as a neurotransmitter. The ganglionic neurons of the sympathetic division primarily release norepinephrine as a neurotransmitter (and both NE and E as hormones at the adrenal medulla). The ganglionic neurons of the parasympathetic division release ACh as a neurotransmitter.

Table 16-2

fig. 16-9

summary and interactions

sympatheticwidespread distribution

parasympatheticvisceral structures served by CNor in abdominopelvic cavity

most organs receive input from both(dual innervation)

actions are usually opposite

anatomy of dual innervation

headparasympathetics with CNsympathetic via superior cevical ganglion

thorax and abdomensympathetics and parasympathetics mix

autonomic plexusescardiacpulmonaryesophagealceliachypogastric

fig. 16-10

autonomic tone

background stimulationallows for more control

two examples:

autonomic tone

1. heart receives dual innervation

review: cardiac muscle has pacemaker

ACh from parasym. slows rateNE from sympath. accelerates rate

both are released all the time but,normally parasym is in control

can modulate heart rate up or down

autonomic tone

2. blood vessel diameter

review: only get sympathetic

background NE from sympathetic

partial constriction of vessels

need more blood stop NE releaseincrease ACh release

blood vessels dilate

autonomic tone

2. blood vessel diameter

review: only get sympathetic

background NE from sympathetic

partial constriction of vessels

need less blood increase NE release

blood vessels constrict

autonomic integration and control

centers are found all over the CNS

primary motor cortex (UMN) …

…LMN of cranial and spinal reflexes

alsovisceral reflexes

example

visceral reflexes

shine a light in one eye…

…both pupils will constrict

parasympathetic

in the dark…

…pupils dilate

sympathetic

(consensual light reflex)

(pupillary reflex)

visceral reflexes

motor muclei controlling the pupils are controlled by hypothalamic centers responding to emotions too

nauseated/queasy pupils constrictsexually aroused pupils dilate


visceral reflex arc

receptor (sensory neuron)processing center (interneurons)two visceral motor neurons

long or short reflexes


long reflexes

equivalent to the spinal reflex (13)

processing (interneurons) in CNS

fig. 16-11


short reflexes

processing (interneurons) in ganglion

bypass the CNS

fig. 16-11


short reflexes

processing (interneurons) in ganglion

bypass the CNS

used extensively in digestive system

ENS


other autonomous reflexes

respiration,cardiovascular,…

table 16-4


other autonomous reflexes

respiration,cardiovascular,…

parasympatheticorgan or

organ system

sympatheticactivated as

a wholedivergance

higher levels of control

centers for:

cardiovascularrespiratory

nuclei in medulla

oblongataswallowingsalivationdigestive secretionsperistalsisurinary functions

hypothalamus

integration of ANS and SNS

see fig. 16-12

Higher order functions

•need cerebral cortex•involve conscious and unconscious•not part of “hardwiring”

subject to modification and adjustment

memory / learningconsciousnesssleep / arousalbrain chemistry / behavioraging


memory / learning

fact memories bit of infoskill memories learned actions

short term (primary)

long termsecondary may fade with timetertiary lifetime

memory consolidation

fig. 16-13


memory / learning


damage hippocampuscannot convert short-term to long-termexisting long term remains intact

involves amygdoloid bodyhippocampus


memory / learning


involves amygdoloid bodyhippocampus

damage to nucleus leads changeswith Alzheimers (later)

nucleus basalis ?


memory / learning


long term memoriesstored the cerebral cortex

association areas

some memories are dependent on the activity of a single neuron

to here 3/19Lec #28


memory / learning


anatomical/physiological neurons and synapses


memory / learning


increased nt releasefacilitation at synapsesadditional synaptic connections

create anatomical changes in circuits

1 circuit/1 memory = memory engram


memory / learning


take time

natureintensityfrequency

of stimulus

strength, extremeness,frequency, drugs

influenced by:


memory / learning


hippocampus

NMDA-receptorschemically gated Ca2+ channels

blocking NMDA receptors prevents formation of long-term memory


memory / learning

amnesia

loss of memory because of disease or trauma


memory / learning

amnesia

retrogradelose memory of past eventse.g., head injury-forget accident

anterogradeinability to store new memoriescommon sign of senilityliving in “new” surroundings


memory / learning

amnesia

can occur suddenly or progresivelyrecovery can be:

completepartialnon-existent

depending on

problem


memory / learning

amnesia

diazepam (valium)Halcion

can cause brief periods of anterograde amnesia

100 Keys (pg. 539)

“Memory storage involves anatomical as well as physiological changes in neurons. The hippocampus is involved in the conversion of temporary, short-term memories into durable long-term memories.”


States of consciousness

conscious----

unconscious

awake

asleep…

coma really asleep


sleep

deep sleepaka., slow wave sleep

non-REM sleep

REM sleeprapid eye movement sleep


sleep

deep sleepbody relaxescerebral activity is minimalheart, resp, bp, energy

utilization all decrease (30%)


sleep

REM sleep

active dreamingresp. rate, bpEEG looks similar to awake, but less response to outside stimulidecrease in muscle tone (intense SNS inhibition) eye muscles escape inhibition


sleep

REM sleep

cycles of REM, non-REM

fig. 16-14a

fig. 16-14b

sleep disorders

25% of Americansabnormal REMsleepwalking

…


sleep


arousal

awakeningcontrolled by the reticular formationextensive interconnections with:

sensorymotorintegrative nuclei


arousal

RASreticular activating system

from medulla to midbrainprojects to thalamus

cortex

activity of cortex is proportionalactivity of RAS

fig. 16-15


arousal

RAS

sleep is ended by activationeffects last short time (min)positive feedback keeps us awake


arousal

RAS

nuclei

nuclei

NE+

serotonin-

promotessleep

maintainsalertness

100 keys (pg. 541)

“An individual’s state of consciousness is variable and complex, rangeing from energized and “hyper” to unconscious and comatose. During deep sleep, all metabolic functions are significantly reduced; during TEM sleep, muscular activities ar inhibited while cerebral activity is similar to that seen in awake individuals. Sleep disorders result in abnormal reaction times, mood swings and behaviors. Awakening occurs when the reticular activating system becomes active; the greater the level of activity, the more alert the individual.”

Brain chemistry and behavior

changes in the balance of nt’s can affect brain function.

sleep-wake cyclesHuntington’s disease


Huntington’s disease

destruction of ACh and GABA secreting neurons in the basal nuclei

loss of basal nuclei, frontal lobes

loss of muscle control and intellectual abilities


serotonin

LSD activates serotonin receptors

hallucinations

enhance serotonin activity


serotonin

block serotonindepression and anxiety

slow serotonin removalincrease serotonin

(SSRI’s)Prozac, Paxil, Zoloft


serotonin

variety of pathways delivering serotonin to nuclei and higher centers

affect sensory interpretation and emotional states


dopamine

needed to reduce muscle tone

stimulated by “speed”causes “schizophrenia”

disturbances inmoodthought andbehavior

Aging

affects all body systems (including brain)changes begin around 30

reduction in brain size and weight (cortex)reduction in # of neurons (cortex)decreased blood flow to brain (arteriosclerosis)changes in synaptic organization (fewer)cellular changes

accumulations inside the cells (tangles)accumulations outside the cells (plaques)

Aging

Alzheimer’s

progressive disorder characterized by loss of higher order cerebral functions

15% of people over 6550% of people over 85100,000 deaths/year

Aging

Alzheimer’s

areas develop “plaques” and “tangles”??

geneticslate onset chromosome 19early onset chromosomes 21 and 14

no cure, but may slow progression

Integration of Nervous System with other body systems

monitors all systemsadjusts their activity

level of impact is variable

skeletal muscle

cardiac muscle

fig. 16-16

Documents

Chapter 16