Physiology of the nervous system

Prof. Vajira Weerasinghe

Professor of Physiology, Faculty of Medicine University of Peradeniya & Consultant Neurophysiologist,

Teaching Hospital, Peradeniya www.slideshare.net/vajira54

Functional Subdivisions• Sensory functions

• feeling, eg. pain

• Motor functions• movement, eg. walking

• Integrative functions• eg. reflexes

• Autonomic functions• control of blood pressure

• Higher functions• memory, learning

Topics

• Action potential • Nerve impulse transmission • Neuromuscular junction • Muscle contraction

• Degeneration and regeneration of nerves

• Autonomic nerve systems • Neurotransmission • Physiology of sensory nervous system • Physiology of motor function

• Physiology of pain and consciousness

• CSF composition, formation and drainage

Excitable tissues

• Excitable tissues have more negative RMP ( - 70 mV to - 90 mV)

excitable Non-excitable

Red cellGIT

neuron

muscle

• Non-excitable tissues have less negative RMP -53 mV epithelial cells-8.4 mV RBC-20 to -30 mV fibroblasts-58 mV adipocytes

Resting Membrane Potential

• This depends on following factors• Ionic distribution across the membrane• Membrane permeability • Other factors

• Na+/K+ pump

Ionic distribution

Ion Intracellular Extracellular

Na+ 10 142

K+ 140 4

Cl- 4 103

Ca2+ 0 2.4

HCO3- 10 28

Flow of Potassium

• Potassium concentration intracellular is more• Membrane is freely permeable to K+

• There is an efflux of K+

K+ K+K+

K+K+ K+

K+

K+

K+K+

Flow of Potassium

• Entry of positive ions in to the extracellular fluid creates positivity outside and negativity inside

K+ K+K+

K+K+ K+

K+

K+

K+K+

Flow of Potassium

• Outside positivity resists efflux of K+

• (since K+ is a positive ion)

• At a certain voltage an equilibrium is reached and K+ efflux stops

K+ K+K+

K+K+ K+

K+

K+

K+K+

Ionic channels

• Leaky channels (leak channels)– Allow free flow of ions– K+ channels (large number) – Na+ channels (fewer in number)– Therefore membrane is more permeable to K+

Na/K pump

• Active transport system for Na+-K+ exchange using energy

• It is an electrogenic pump since 3 Na+ efflux coupled with 2 K+ influx

• Net effect of causing negative charge inside the membrane

3 Na+

2 K+

ATP ADP

Factors contributing to RMP

• One of the main factors is K+ efflux (Nernst Potential: -90mV)

• Contribution of Na+ influx is little (Nernst Potential: +60mV)

• Na+/K+ pump causes more negativity inside the membrane

• Negatively charged protein ions remaining inside the membrane contributes to the negativity

• Net result: -70 to -90 mV inside

Action Potential (A.P.)

• When an impulse is generated– Inside becomes positive – Causes depolarisation– Nerve impulses are

transmitted as AP

Dep

olar

isat

ion R

epolarisation

-70

+30

RMP

Hyperpolarisation

• Sub-threshold stimulus No action potential

• Threshold stimulus Action potential is triggered

• Supra-threshold stimulus Action potential is triggered

• Strength of the stimulus above the threshold is coded as the frequency of action potentials

Physiological basis of AP

• When the threshold level is reached– Voltage-gated Na+ channels open up– Since Na+ conc outside is more than the inside– Na+ influx will occur– Positive ion coming inside increases the positivity of the

membrane potential and causes depolarisation

-70

+30

outside

inside

Na+Voltage-gated Na+ channel

Physiological basis of AP

– When membrane potential reaches +30, Na+ channels are inactivated

– Then Voltage-gated K+ channels open up– K+ efflux occurs– Positive ion leaving the inside causes more negativity inside

the membrane– Repolarisation occurs

-70

+30

outside

inside

At +30

K+

Hyperpolarisation

• When reaching the Resting level rate slows down

• Can go beyond the resting level– Hyperpolarisation

• (membrane becoming more negative)

-70

+30

Role of Na+/K+ pump

• Since Na+ has come in and K+ has gone out

• Membrane has become negative

• But ionic distribution has become unequal

• Na+/K+ pump restores Na+ and K+ conc slowly– By pumping 3 Na+ ions outward and 2+ K ions

inward

Propagation of AP

• When one area is depolarised

• A potential difference exists between that site and the adjacent membrane

• A current flow is initiated

• Current flow through this local circuit is completed by extra cellular fluid

Propagation of AP

• This local current flow will cause opening of voltage-gated Na+ channel in the adjacent membrane

• Na+ influx will occur

• Membrane is depolarised

Propagation of AP

• Then the previous area become repolarised

• This process continue to work

• Resulting in propagation of AP

Propagation of AP

Propagation of AP

Propagation of AP

Propagation of AP

Propagation of AP

Propagation of AP

Propagation of AP

Propagation of AP

AP propagation along myelinated nerves

• Na+ channels are conc around nodes

• Therefore depolarisation mainly occurs at nodes

Distribution of Na+ channels

• Number of Na+ channels per square micrometer of membrane in mammalian neurons

50 to 75 in the cell body350 – 500 in the initial

segment < 25 on the surface

of myelin 2000 – 12,000 at the nodes of

Ranvier20 – 75 at the axon

terminal

AP propagation along myelinated nerves

• Local current will flow from one node to another• Thus propagation of action potential and therefore nerve

conduction through myelinated fibres is faster than unmyelinated fibre – Conduction velocity of thick myelinated A alpha fibres is

about 70-100 m/s whereas in unmyelinated fibres it is about 1-2 m/s

Skeletal muscle

• Skeletal muscle is supplied by somatic nerve

• When there is a signal to the muscle it contracts and relaxes

• Thus there are two events in the skeletal muscle – Electrical - action potential – Mechanical - contraction

Muscle contraction

• Excitation - contraction coupling

– Excitation : electrical event– Contraction : mechanical event

Mechanical event follows electrical event

Skeletal muscle

• Electrical event in a skeletal muscle membrane is exactly similar to nerve action potential

• Same duration = 1 msec

• Same voltage difference = from -70 to +30 mV

Effect of serum hypocalcaemia • Concentration of calcium in ECF has a

profound effect on voltage level at which Na+ channels activated

• Hypocalcaemia causes hyperexcitability of the membrane

• When there is a deficit of Ca2+ (50% below normal) sodium channels open (activated) by a small increase in the membrane potential from its normal level – Ca2+ ions binds to the Na+ channel and alters the

voltage sensor

Effect of serum hypocalcaemia

• Therefore membrane becomes hyperexcitable

• Sometimes discharging spontaneously repetitively

– tetany occurs

• This is the reason for hypocalcaemia causing tetany

NMJ function

• Pre-synaptic membrane• Ca channels• Acetycholine release

• Postsynaptic membrane• Acetylcholine receptors• Ligand-gated channels

• Synaptic cleft• cholinesterase

Presynaptic terminal (terminal knob, boutons, end-feet or synaptic knobs)♦ Terminal has synaptic vesicles and mitochondria

♦ Mitochondria (ATP) are present inside the presynaptic terminal

Vesicles containing neurotransmitter (Ach)

Presynaptic terminal (terminal knob, boutons, end-feet or synaptic knobs)♦ Presynaptic membrane contain voltage-gated Ca2+ channels

♦ The quantity of neurotransmitter released is proportional to the number of Ca2+ entering the terminal

♦ Ca2+ ions binds to the protein molecules on the inner surface of the synaptic membrane called release sites

♦ Neurotransmitter binds to these sites and exocytosis occur

Ca2+ Ca2+

• Postsynaptic membrane contain nicotinic acetylcholine receptor

AchNa+

•This receptor contains several sub units (2 alpha, beta, delta & epsilon)

•Ach binds to alpha subunit

•Na+ channel opens up

•Na+ influx occurs

NMJ blocking

• Useful in general anaesthesia to facilitate inserting tubes

• Muscle paralysis is useful in performing surgery

Neuromuscular blocking agents

• Non-depolarising type (competitive)– Act by competing with Ach for the Ach receptors– Binds to Ach receptors and blocks– Prevent Ach from attaching to its receptors– No depolarisation– Late onset, prolonged action – 70–80% of receptors should be occupied to produce an effect – To produce complete block, at least 92% of receptors must be occupied – Ach can compete & the effect overcomes by an excess Ach– Anticholinesterases can reverse the action– eg.

• Curare• Atracurium• Tubocurarine

Neuromuscular blocking agents

• Depolarising type (non-competitive)– Act like Ach, but resistant to AchE action– Bind to motor end plate and once depolarises – Persistent depolarisation leads to a block

• Due to inactivation of Na channels– Two phases

• Phase I – depolarisation phase – fasciculations • Phase II – paralysis phase

– Ach cannot compete– Quick action start within 30 sec, recover within 3 min and is

complete within 12–15 min – Anticholinesterases cannot reverse the action– eg.

• Succinylcholine • Ach in large doses• Nicotine

Anticholinesterases• AchE inhibitors

– Inhibit AchE so that Ach accumulates and causes depolarising block

• Reversible– Competitive inhibitors of AChE– Block can be overcome by curare

• physostigmine, neostigmine, edrophonium

• Irreversible– Binds to AChE irreversibly

• , insecticides, nerve gases

NMJ disorders

• Myasthenia gravis – Antibodies to Ach receptors– Post synaptic disorder

• Lambert Eaton Syndrome (myasthenic syndrome)– Presynaptic disorder (antibodies against Ca channels)

• Botulism– Presynaptic disorder

– Binds to the presynatic region and prevent release of Ach

Differences between sympathetic and Differences between sympathetic and parasympathetic nervous systems parasympathetic nervous systems

Ach (N)

Ach (N) Ach (M)

Nor

Sympathetic

Parasympathetic

Adre

Neurotransmitters and ReceptorsNeurotransmitters and Receptors

► Acetylcholine (ACh) and norepinephrine (NE) are the Acetylcholine (ACh) and norepinephrine (NE) are the two major neurotransmitters of the ANStwo major neurotransmitters of the ANS

► ACh is released by all preganglionic axons and all ACh is released by all preganglionic axons and all parasympathetic postganglionic axonsparasympathetic postganglionic axons

► Cholinergic f ibersCholinergic f ibers – ACh-releasing fibers – ACh-releasing fibers ► Adrenergic f ibersAdrenergic f ibers – sympathetic postganglionic – sympathetic postganglionic

axons that release NE axons that release NE

► Neurotransmitter effects can be excitatory or inhibitory Neurotransmitter effects can be excitatory or inhibitory depending upon the receptor typedepending upon the receptor type

Nicotinic Receptors (cholinergic)Nicotinic Receptors (cholinergic)

►Nicotinic receptors are found on:Nicotinic receptors are found on: Motor end plates (somatic targets)Motor end plates (somatic targets) All ganglionic neurons of both sympathetic All ganglionic neurons of both sympathetic

and parasympathetic divisionsand parasympathetic divisions The hormone-producing cells of the The hormone-producing cells of the

adrenal medullaadrenal medulla

►The effect of ACh binding to nicotinic The effect of ACh binding to nicotinic receptors is receptors is always stimulatoryalways stimulatory

Muscarinic Receptors Muscarinic Receptors (cholinergic) (cholinergic)

►Muscarinic receptors occur on all effector Muscarinic receptors occur on all effector cells stimulated by postganglionic cells stimulated by postganglionic cholinergic fiberscholinergic fibers

►The effect of ACh binding: The effect of ACh binding: Can be either inhibitory or excitatoryCan be either inhibitory or excitatory Depends on the receptor typeDepends on the receptor type of the of the

target organtarget organ

Adrenergic ReceptorsAdrenergic Receptors

► The two types of adrenergic receptors are alpha The two types of adrenergic receptors are alpha and betaand beta

► Each type has two or three subclasses Each type has two or three subclasses ((αα11, , αα22, , ββ11, , ββ2 2 , , ββ33))

► Effects of NE binding to: Effects of NE binding to: αα receptors is generally stimulatoryreceptors is generally stimulatory ββ receptors is generally inhibitoryreceptors is generally inhibitory

► A notable exception – NE binding to A notable exception – NE binding to ββ receptors of receptors of the heart is stimulatorythe heart is stimulatory

Alpha ReceptorsAlpha Receptors► Alpha 1: adrenergic receptors located on Alpha 1: adrenergic receptors located on

postsynaptic effector cells.postsynaptic effector cells. Smooth muscles of blood vessels: ConstrictionSmooth muscles of blood vessels: Constriction

► Arteriolar constrictionArteriolar constriction Bladder sphincterBladder sphincter PenisPenis Uterus Uterus Pupillary muscles of irisPupillary muscles of iris

► Alpha 2Alpha 2 Same as the Alpha 1 but are located in the presynaptic Same as the Alpha 1 but are located in the presynaptic

nerve terminalsnerve terminals

Adrenergic ReceptorAdrenergic Receptor

►Beta 1Beta 1►CardiovascularCardiovascular

Cardiac muscle: increased contractilityCardiac muscle: increased contractilityincreased force of contraction increased force of contraction

Atrioventricular node: increased heart rateAtrioventricular node: increased heart rate Sinoatrial node: increase in heart rateSinoatrial node: increase in heart rate

►EndocrineEndocrine PancreasPancreas

Adrenergic ReceptorAdrenergic Receptor

►Beta 2Beta 2►CardiovascularCardiovascular

Dilation of blood vesselsDilation of blood vessels►EndocrineEndocrine►Uterine relaxationUterine relaxation►Respiratory: dilation of bronchial musclesRespiratory: dilation of bronchial muscles

HeartHeart

►Direct stimulation of receptorsDirect stimulation of receptors Alpha 1 – Alpha 1 –

►Vasoconstriction of blood vessels which increases Vasoconstriction of blood vessels which increases blood pressureblood pressure

►Pressor or vasopressor effect to maintain blood Pressor or vasopressor effect to maintain blood pressurepressure

Beta 1Beta 1►Increased force of myocardial contraction Increased force of myocardial contraction ►Increased speed of electrical conduction in the heart.Increased speed of electrical conduction in the heart.

Sensory Functions

• General Sensations

• Special Sensations• Vision• Hearing• Taste• Smell

Receptor

Sensory modality

Sensory nerve

Central Connections

Ascending Sensory pathway

Sensory area in the brain

Touch stimulus

AFFERENT

Classification of receptors

• Mechanoreceptors

• Thermoreceptors

• Nociceptors• pain

• Chemoreceptors• taste, smell, visceral

• Electromagnetic receptors• visual

Mechanoreceptors

• Mainly cutaneous• Touch• Pressure• Vibration

• Crude or Fine mechanosensations

• Others: auditory, vestibular, stretch

What happens inside a receptor?

• TRANSDUCTION• Stimulus energy is converted to action

potentials• Inside the nervous system signals are always

action potentials

• Language of the nervous system contains only 1 word: action potentials

• At the brain opposite happens in order to feel the sensation• PERCEPTION

Two ascending pathways

• Dorsal column - medial lemniscus pathway

fast pathway

• Spinothalamic pathwayslow pathway

These two pathways come together at the level of thalamus

Dorsal column pathwaySpinothalamic pathway

Lateral Spinothalamic tract

AnteriorSpinothalamic tract

Dorsal column pathway Spinothalamic pathway

• touch: fine degree

• highly localised touch sensations

• vibratory sensations• sensations signalling

movement• position sense

• pressure: fine degree

• Pain

• Thermal sensations• Crude touch &

pressure• crude localising

sensations• tickle & itch

• sexual sensations

Dorsal column nuclei(cuneate & gracile nucleus)

Dorsal column

Medial lemniscus

thalamus

thalamocortical tracts

sensory cortex

internal capsule

1st order neuron

2nd order neuron

3rd order neuron

Spinothalamic tracts

thalamus

thalamocortical tracts

sensory cortex

internal capsule

1st order neuron

2nd order neuron

3rd order neuron

Abnormalities• Sensory loss• Anaesthesia

• absence of sensation

• Paraesthesia• abnormal sensation

• Hemianaesthesia• Loss of sensation of one half of the body

• Astereognosis

Localisation of the abnormality• Peripheral nerve

• part of a limb is affected

• Roots• dermatomal pattern of sensory loss

• spinal cord• a sensory level

• internal capsule• one half of the body

What is a reflex?

Stimulus

Effector organ

Response

Centralconnections

Efferent nerve

Afferent nerveReceptor

Stretch reflex

• This is a basic reflex present in the spinal cord• Stimulus: muscle stretch• Response: contraction of the muscle

• Receptors: stretch receptors located in the muscle spindle

• Importance of stretch reflex• Detects muscle length and changes in muscle length

Ia afferent nerve

α motor neuronone

synapse

muscle stretchmuscle

contraction γ Motor neuron

Motor system

• Consists of • Upper motor neuron• Lower motor neuron

Medulla

motor cortex

internal capsule

Uppermotorneuron

Lowermotorneuron

anterior horn cell

alpha motor neuron

• this is also called the final common pathway

• Contraction of the muscle occurs through this whether • voluntary contraction through corticospinal

tract

or• involuntary contraction through gamma

motor neuron - stretch reflex - Ia afferent

• Lower motor neuron lesion causes• flaccid paralysis

• Upper motor neuron lesion causes• spastic paralysis

Lower motor neuron lesion

• muscle weakness

• flaccid paralysis

• muscle wasting (disuse atrophy)

• reduced muscle tone (hypotonia)

• reflexes: reduced or absent

• spontaneous muscle contractions (fasciculations)

• plantar reflex: flexor

• superficial abdominal reflexes: present

Upper motor neuron lesion

• muscle weakness

• spastic paralysis

• increased muscle tone (hypertonia)

• reflexes: exaggerated

• Babinski sign: positive

• superficial abdominal reflexes: absent

• muscle wasting is very rare

Cerebellum

• Centre of motor coordination

• Cerebellar disorders cause incoordination or ataxia

• Functions of cerebellum • Planning of movements• Timing & sequencing of movements• Particularly during rapid movments such as during walking, running• From the peripheral feedback & motor cortical impulses, cerebellum

calculates when does a movement should begin and stop

Features of cerebellar disorders• ataxia

• incoordination of movements

• ataxic gait• broad based gait• leaning towards side of the lesion

• dysmetria• cannot plan movements

• past pointing & overshoot

• decomposition of movements• intentional tremor• dysdiadochokinesis

• unable to perform rapidly alternating movements• dysarthria

• slurring of speech

• dysphagia• swallowing difficulty

• nystagmus

• oscillatory movements of the eye• hypotonia

• reduction in tone• due to excitatory influence on gamma motor neurons by cerebellum (through vestibulospinal tracts)

• decreased reflexes• head tremor• head tilt

Basal ganglia• These are a set of deep nuclei located in and around the basal

part of the brain• Caudate nucleus• Putamen• Globus pallidus• Substantia nigra• Subthalamic nuclei

• Basal ganglia disorders• Parkinsonism• Athetosis• Chorea• Hemiballismus

Parkinsonism• due to destruction of dopamine secreting pathways

from substantia nigra to caudate and putamen.• also called paralysis agitans• first described by Dr. James Parkinson in 1817.

Clinical features:

• Rigidity of all the muscles

• Akinesia (bradykinesia): very slow movements, sluggish to initiate

• Resting tremor

• Normal muscle power

• expressionless face• flexed posture• soft, rapid, indistinct speech• slow to start walking• rapid, small steps, tendency to run• reduced arm swinging• impaired balance on turning• resting tremor (4-6 Hz) (pill-rolling tremor)

• diminishes on action

• cogwheel rigidity• lead pipe rigidity• impaired fine movements• impaired repetitive movements

maintenance of posture• mainly to maintain the static posture• necessary for the stability of

movements• involve a set of reflexes• integrated at spinal cord, brain stem

and cortical level

Postural reflexes• stretch reflex• positive supporting reaction (magnet reaction)• negative supporting reaction• mass reflex

• tonic labyrinthine reflex

• tonic neck reflexes

• labyrinthine righting reflex• neck righting reflex• body-on-head righting reflex

• body-on-body righting reflex

• optical righting reflex

• placing reactions• hopping reaction

postural adjustments

vestibular nucleicerebellum

pressure& otherreceptors

neckreceptors

Retina Occulomotor system vestibularsystem

complex pathways

idea•premotor area•supplementary motor area

motor cortex movement

basal ganglia

cerebellum cerebellum

plan execute

memory, emotions

What is pain?• There is an International definition of pain

formulated by the IASP (International Association for the study of pain)

• Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

IASP – International Association for the Study of Pain 2011

• Nociceptive pain

• Neuropathic pain

• Psychogenic pain

• Transduction– Process of converting noxious stimulus to action

potentials

• Perception– Central processing of nociceptive impulses in order

to interpret pain

Dual nature of painfast and slow pain

• fast pain

– acute

– pricking type

– well localised

– short duration– Aδ fibres are involved– fast conduction 20 m/s– somatic pain

• slow pain

– chronic

– throbbing type

– poorly localised

– long duration– unmyelinated C fibres are

involved– slow conduction 1-2 m/s– visceral pain

lateralspinothalamic tract

thalamus

sensory cortex

C fibre

thalamocorticaltracts

Descending pain modulatory system

• several lines of experimental evidence show the presence of descending pain modulatory system

– discovery of morphine receptors– they were known to be present in the brain

stem areas

– discovery of endogenous opioid peptides

• eg. Endorphines, enkephalins, dynorphin

Gate control theory

• This explains how pain can be relieved very quickly by a neural mechanism

• First described by P.D. Wall & Melzack (1965)

• “There is an interaction between pain fibres and touch fibre input at the spinal cord level in the form of a ‘gating mechanism’

Gate control theory

central control

transmission cell

touch

Aβ fibre

when C fibre is stimulated, gate will be opened & pain is felt

pain

C & Aδ fibres

pain is felt

+gate is opened

Gate control theory

central control

transmission cell

when Aβ & C fibres are stimulated together, gate will be closed & pain is not felt

pain is

not felt

touch

Aβ fibre

pain

C & Aδ fibres

+ -

gate is closed

Consciousness • Consciousness is the state of being awake and aware of one's

surroundings

• Assessed by observing a patient's alertness and responsiveness, and can been seen as a continuum of states ranging from – alert – oriented to time and place– communicative– disorientation– delirium– loss of any meaningful communication– loss of movement in response to painful stimulation

• Glasgow Coma Scale (GCS) clinically measures the degree of consciousness

Sleep• A natural periodic state of rest for the

mind and body, in which the eyes usually close and there is a decrease in bodily movement and responsiveness to external stimuli

• Whether it is a state of unconsciousness is questionable

• coma is an unconscious state from which the person cannot be aroused

• In general anaesthesia a patient is deliberately put into a state of unconsciousness under the action of centrally acting drugs

Arousal & Reticular Activating System

• Keeping in conscious, alert, awake state. Is a function of RAS.

• In parallel with the ascending somatosensory tracts through thalamus to cortex.

• There is a more diffuse ascending system consisting mostly of the ascending reticular formation and diffuse nuclei of the thalamus.

• This RAS is necessary to maintain a general level of excitability in the cortex.

Reticular formation

CSF

• Cerebral blood flow: 750 ml/min (15% of cardiac output)

• volume of CSF– 150 ml

• rate of production

– 500 ml/day

• formed

– mainly in the choroid plexuses of the ventricles

– small amounts in the ventricles, arachnoid membranes & perivascular spaces

formation• choroid plexus projects into

– horn of lateral ventricle– posterior portion of 3rd ventricle– roof of the 4th ventricle

• Mechanism:– active transport of Na through the epithelial

cells, Cl follows passively– osmotic outflow of water– glucose moves in to CSF– K and HCO3 moved out of CSF

composition

• similar to plasma– CSF Plasma– Na 147 (similar) 150 mmol/l– K 2.9 (less) 4.6 mmol/l– HCO3 25 24.8 mmol/l– Cl 113 (more) 99 mmol/l– Pco2 50 40 mmHg– pH 7.33 7.4– osmolality 289 (similar) 289 mosm– protein 20 (less) 6000 mg/dl– glucose 64 (less) 100 mg/dl– urea 12 (less) 15 mg/dl

• some substances do not pass into CSF

blood brain barrier

• tight junctions between capillary endothelial cells & epithelial cells in the choroid prevent some substances entering CSF

• small molecules & lipid soluble substances pass through easily

• blood-brain barrier exists between blood & brain tissue

• blood-CSF barrier is present in choroid

• these barriers are– highly permeable to water, CO2, O2, lipid soluble

substances (such as alcohol), most anaesthetics, – slightly permeable to electrolytes– impermeable to proteins, large organic molecules– drugs (variable)

blood brain barrier

• CO2 & O2 crosses easily• H+ & HCO3- slow penetration• glucose

– passive: slow penetration– active transport system by glucose transporter GLUT

• Na-K-Cl transporter

• transporters for other substances

blood brain barrier

– No blood brain barrier in the hypothalamus & posterior pituitary

• substances diffuses easily• these areas contain chemoreceptors for various

substances to detect changes in conc

brain metabolism

– brain metabolism is 15% of total metabolism of the body (although brain mass is 2% of total body mass)

– therefore brain has an increased metabolic rate– this is due to increased activity of neurons (AP)– requires oxygen– brain is not capable of anaerobic metabolism– energy supply is by glucose – glucose entry is not controlled by insulin

Nerve degeneration and regeneration

• Demyelination

• Axonal degeneration

• Remyelination

• Axonal regeneration