md ophth neurophysiology
TRANSCRIPT
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