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Nerve conduction Neurotransmitters NMJ.pptx
1. Nerve conduction,
Neurotransmitters and
Neuromuscular Junction
Prof. Vajira Weerasinghe
Senior Professor of Physiology
Department of Physiology, Faculty of Medicine,
University of Peradeniya and Consultant Neurophysiologist,
Teaching Hospital Peradeniya
www.slideshare.net/vajira54
2. ILO
• Describe Neurotransmitters
• Describe Neuromuscular transmission
• Describe Basic structure of neuromuscular junction
• Identify Disorders of neuromuscular transmission
• Define Different types of nerve conduction
• Describe Alteration in nerve conduction in nerve
injuries
3. Synapse
• Synapse is a gap between two neurons
• More commonly chemical
• Rarely they could be electrical (with gap
junctions)
• which are pores (as shown in the electron
micrograph) constructed of connexin proteins
7. Types of synapses
• Axo-dendritic synapse
• Most common
• Axon terminal branch (presynaptic element)
synapses on a dendrite
• Axo-somatic synapse
• Axon terminal branch synapses on a soma (cell
body)
• Axo-axonic synapse
• Axon terminal branch synapses on another axon
terminal branch (for presynaptic inhibition)
• Dendro-dendritic synapse
• Dendrite synapsing on another dendrite
(localised effect)
8. • Axo-dendritic synapse
• Most common
• Axon terminal branch
(presynaptic element)
synapses on a dendrite
• Axo-somatic synapse
• Axon terminal branch
synapses on a soma (cell
body)
• Axo-axonic synapse
• Axon terminal branch
synapses on another axon
terminal branch (for
presynaptic inhibition)
• Dendro-dendritic synapse
• Dendrite synapsing on
another dendrite (localised
effect)
9. Synaptic ultrastructure
• The presynaptic
enlargement (bouton,
varicosity, or end
plate) contains
synaptic vesicles (20
nm diameter) and
synaptic protein
chains
• Pre- and postsynaptic
plasma membranes are
separated by a
synaptic cleft (20 nm
wide)
• The cleft contains
glycoprotein linking
material and is
surrounded by glial
cell processes
Synaptic
proteins
10. Presynaptic events
• Presynaptic membrane contains
voltage gated calcium
channels
• Membrane depolarisation opens
up Ca2+ channels
• Ca2+ influx will occur
• Neurotransmitter molecules
are released in proportion to
the amount of Ca2+ influx, in
turn proportional to the
amount of presynaptic
membrane depolarization
11. Details of
presynapti
c events
• in the resting state, the presynaptic membrane
has resting membrane potential
• when an action potential arrives at the end of
the axon
• the adjacent presynaptic membrane is depolarised
• voltage-gated Ca2+ channels open and allow Ca2+
influx (driven by [Ca2+] gradient)
• elevated [Ca2+] activates synaptic proteins
(SNARE proteins: Synaptobrevin, Syntaxin, SNAP
25) and triggers vesicle mobilization and docking
with the plasma membrane
• vesicles fuse with presynaptic plasma membrane
and release neurotransmitter molecules (about
5,000 per vesicle) by exocytosis
• neurotransmitter molecules diffuse across the
cleft & bind with postsynaptic receptor proteins
• neurotransmitter molecules are eliminated from
synaptic clefts via pinocytotic uptake by
presynaptic or glial processes and/or via
enzymatic degradation at the postsynaptic
membrane
12. Synaptic
transmission
Action potential passes from the
presynaptic neuron to the
postsynaptic neuron
Although an axon conducts both
ways, conduction through synapse
is one way
(retrograde transmission also can
occur)
A neuron receives more than 10000
synapses
Postsynaptic activity is an
integrated function
13. Neurotransmitters
• Chemicals that facilitate signal transmission
across a synapse
• Neurotransmitters are released on the
presynaptic side and bind to receptors on the
postsynaptic side
• Earliest neurotransmitter discovered was
acetylcholine
• There are different chemical types
• Amines
• Norepinephrine, Epinephrine, dopamine, serotonin (5HT),
histamine
• Amino acids
• GABA, Glycine, Glutamate, Aspartate
• Peptides
• Beta endorphin, enkephalins, dynorphin
14. Neurotransmitter release
• “At rest”, the synapse contains numerous
synaptic vesicles filled with neurotransmitter
• Intracellular calcium levels are very low
• Arrival of an action potential causes opening
of voltage-gated calcium channels
• Calcium enters the synapse
• Calcium triggers exocytosis and release of
neurotransmitter
• Vesicles are recycled by endocytosis
15. Neurotransmitter receptors
• Once released, the neurotransmitter molecules
diffuse across the synaptic cleft
• When they “arrive” at the postsynaptic
membrane, they bind to neurotransmitter
receptors
• Two main classes of receptors:
• Ionotropic receptors
• Metabotropic receptors
16. IONOTROPIC RECEPTORS
• Neurotransmitter molecule binds to the receptor
• Cause a ligand-gated ion channel to open
• Become permeable to either sodium, potassium or chloride
• Accordingly depolarisation (excitation) or hyperpolarisation (inhibition)
• Quick action, short lasting
17. Metabotropic
Receptors
• Neurotransmitter attaches to G-
protein-coupled receptors (GPCR)
which has slower, longer-lasting and
diverse postsynaptic effects
• They can have effects that change an
entire cell’s metabolism
• Activates enzymes that trigger
internal metabolic change inside the
cell
• Activate cAMP
• Activate cellular genes: forms more
receptor proteins
• Activate protein kinase: decrease
the number of proteins
• Sometimes open up ion channels also
18. • Excitation
• 1. Na+ influx cause accumulation of positive charges
causing excitation
• 2. Decreased K+ efflux or Cl- influx
• 3. Various internal changes to excite cell, increase
in excitatory receptors, decrease in inhibitory
receptors.
19. • Inhibition
• 1. Efflux of K+
• 2. Influx of Cl-
• 3. activation of receptor enzymes to inhibit
metabolic functions or to increase inhibitory
receptors or decrease excitatory receptors
20. • Excitatory effects of neurotransmitters
• EPSP: excitatory post synaptic potential
• Inhibitory effects of neurotransmitters
• IPSP: inhibitory post synaptic potential
21. Postsynaptic activity
• Synaptic integration
• On average, each neuron in the brain receives about
10,000 synaptic connections from other neurons
• Many (but probably not all) of these connections may
be active at any given time
• Each neuron produces only one output
• One single input is usually not sufficient to
trigger this output
• The neuron must integrate a large number of synaptic
inputs and “decide” whether to produce an output or
not
23. Neuromuscular junction
• This is a modified
synapse
• Consists of
• Presynaptic membrane
(nerve terminal)
• Synaptic cleft
• Postsynaptic membrane
(motor end plate)
24.
25. 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)
26. Presynaptic terminal (terminal knob,
boutons, end-feet or synaptic knobs)
Presynaptic membrane contain voltage-gated Ca
channels
The quantity of neurotransmitter released is
proportional to the number of Ca entering the
terminal
Ca 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
28. Ach vesicle docking
• With the help of Ca entering the presynaptic terminal
• Docking of Ach vesicles occur
• Docking:
• Vesicles move toward & interact with membrane of presynaptic
terminal
• There are many proteins necessary for this purpose
• These are called SNARE (soluble NSF attachment protein
receptor) proteins
• Syntaxin, synaptobrevin, SNAP25
• Botulinum toxin cleaves all three SNARE proteins
• Tetanus toxin causes cleavage of synaptobrevin
29.
30. Ach release
• An average human end plate contains 15-40
million Ach receptors
• Each nerve impulse release 60 Ach vesicles
• Each vesicle contains about 10,000 molecules of
Ach
• Ach is released in quanta (small packets)
31. NMJ
• Postsynaptic membrane contain nicotinic
acetylcholine receptor
• This receptor contains several
sub units (2 alpha, beta, gamma,
delta)
• Ach binds to alpha subunit
• Na+ channel opens up
• Na+ influx occurs
• End Plate Potential (EPP)
•This is a graded potential
•Once this reaches the threshold
level
•AP is generated at the
postsynaptic membrane
32. • Na+ influx causes depolarisation of the
membrane
• End Plate Potential (EPP)
• This is a graded potential
• Once this reaches the threshold level
• AP is generated at the postsynaptic membrane
33. End plate potential
• Even at rest small quanta are released
• Which creates a minute depolarising spike
called Miniature End Plate Potential (MEPP)
• When an impulse arrives at the NMJ quanta
released are increased in several times causing
EPP
34. Acetylcholinerase (AchE)
• After the Ach binding is over
• Cholinesterase present in the synaptic cleft
will hydrolyse Ach into choline and acetate
• Choline is reuptaken to the presynaptic
terminal
• AchE is also found in RBC membranes
35. Situatio
ns where
NMJ
blocking
occurs
1. In the animal world to kill a prey snake
uses poison which contains NMJ blocker
2. South American hunters used arrow poison
to kill animals and the arrow poison contains NMJ blocking
property
3. In suicide commonest poison used is insectide which is an
organophosphate which has NMJ blocking property
4. Useful in general anaesthesia to facilitate inserting tubes
5. Muscle paralysis is useful in performing surgery
6. In serious neuromuscular disorder called myasthenia gravis NMJ
blocking occurs
7. Miracle drug – botulinum toxin works by blocking NMJ
36. Earliest known NMJ blocker - Curare
• Curare has long been used in South
America as an extremely potent arrow
poison
• Darts were tipped with curare and
then accurately fired through
blowguns made of bamboo
• Death for birds would take one to
two minutes, small mammals up to ten
minutes, and large mammals up to 20
minutes
• NMJ blocker used in patients is
tubocurarine
37. Competitive NMJ blockers
(Non-depolarising NMJ
blockers)
• eg.
• Curare
• Atracurium
• Rocuronium
• Vencuronium
• Competitive or non-depolarizing type
• Physically similar to Ach but no chemical (ligand) action
• 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
• Ach can compete & the effect overcomes by an excess Ach
• Anticholinesterases can reverse the action by destroying
cholinesterase and increasing Ach level
38. Depolarising NMJ blockers
(Non-competitive NMJ blockers)
• eg. Succinylcholine
• non-competitive, chemically act like Ach
• Bind to motor end plate and once depolarizes
• Not easily removed by acetylcholinesterase
• Persistent depolarisation leads to a block
• Due to inactivation of Na channels
• Ach cannot compete with depolarising blockers
• Succinylcholine has quick action start within 1 min and last
for 12 min
• Hydrolysed by plasma cholinesterase (also called
pseudocholinesterase) produced in the liver
42. Repolarized
PHASE II
Membrane repolarizes
but the receptor is
desensitized to effect
of acetylcholine
+ + + +
- - - -
+ + + +
- - - -
- - - -
+ + + +
- - - -
+ + + +
Depolarizing Neuromuscular blocking drugs
43. Anticholinesterases
• AchE inhibitors
• Inhibit AchE so that Ach accumulates and causes
depolarising block
• Reversible
• Competitive inhibitors of AChE
• eg. physostigmine, neostigmine, edrophonium used to
diagnose and treat myasthenia
• Irreversible
• Binds to AChE irreversibly
• eg. Insecticides (organophosphates), nerve gases
(sarin)
44. Organophosphates
• Phosphates used as
insecticides
• Action
• AchE inhibitors
• Therefore there is an excess
Ach accumulation
• Depolarising type of
postsynaptic block
• Used as a suicidal poison
• Causes muscle paralysis and
death
• Nerve gas (sarin)
45. Snake venom
• Common Krait (bungarus
caeruleus)
• Produces neurotoxin known as
bungarotoxin
• Very potent
• Causes muscle paralysis and
death if not treated
• Cobra
• venom contain neurotoxin
46. Myasthenia gravis
• Neuromuscular disease
• Antibodies form against acetylcholine
nicotinic postsynaptic receptors at the
NMJ
• Characteristic pattern of progressively
reduced muscle strength with repeated use
of the muscle and recovery of muscle
strength following a period of rest
• Present with ptosis, fatiguability,
speech difficulty, respiratory difficulty
• Treated with cholinesterase inhibitors
48. Acetylcholine (Ach)
• earliest neurotransmitter discovered
• secreted at the following sites
• neuromuscular junction (skeletal muscle contraction
excitatory)
• heart (inhibitory)
• autonomic ganglia (both sympathetic and parasympathetic)
• adrenal medulla
• parasympathetic postganglionic nerve endings
• central pathways in the brain (neocortex, hippocampus) and
basal forebrain (cognition, memory, arousal, attention)
• brainstem (REM sleep)
• large pyramidal cells of the motor cortex
• basal ganglia (striatum)
• receptors
• nicotinic (NN: autonomic ganglia, NM: NMJ) – ionotropic
receptors Na+ influx
• muscarinic (parasympathetc terminal)
• sub types: M1, M2, M3, M4, M5
• metabotropic receptors with G protein and second
messenger cAMP and K+ channel opening
49. Glutamate
• The most abundant and the main excitatory neurotransmitter in the brain
(70% of all synapses)
• Does not cross BBB, synthesised at the nerve terminal using glutamine
secreted from glial cells
• Ca2+ is necessary for release
• Reuptake to the presynaptic terminal or glial cells by excitatory amino
acid transporter (EAAT)
• receptors
• Ionotropic receptors
• NMDA, AMPA and Kainate receptors
• NMDA receptor is normally blocked by Mg2+, membrane
depolarisation removes Mg2+, then glutamate binds to NMDA
receptor with the co-activator glycine.
• open up Na+ Ca2+ (K+) channels, Ca2+ influx, activates protein
kinases and several actions
• Metabotropic receptors: G protein coupled second messenger system,
act thru inositol phosphate and cAMP, opens up Na+ channel and
other intracellular events
• Important for learning and memory functions and pain
mechanism
• Have been implicated in neurological disorders such as
stroke, epilepsy, Alzheimer's disease
50. GABA
• The main inhibitory neurotransmitter in the brain (occurring in
about 40% of all synapses
• Causes both presynaptic and postsynaptic inhibition
• Reuptake up GABA transporter
• receptors
• GABA A receptor (ionotropic): postsynaptic, open up Cl-
channel, hyperpolarisation, inhibition, alcohol,
antiepieptics (barbirurates), benzodiazepine (diazepam),
activate these receptors
• GABA B receptor (metabotropic): presynaptic , G protein
coupled action, increase K+ efflux, inhibit Ca2+ influx
through presynaptic Ca2+ channels
• GABA C receptor is also known to be present
• Increased GABA activity causes sedative effect
• Main neurotransmitter which produces SWS sleep
• GABA decreases serotonergic, noradrenergic, cholinergic and
histaminergic neuronal activity
• Secreted by the neurons originating in striatum terminating in
globus pallidus & substantia nigra. Also present in the spinal
cord, cerebellum & many other areas of the Cx
51. Dopamine
• Dopamine (DA) is present in several important areas and pathways in the
brain involved in reward pathway
• Ventral tegmental area (VTA) of the midbrain
• Nucleus accumbens (NA) of basal forebrain (brain pleasure centre)
• Mesocortical pathway from midbrain to prefrontal cortex
• Mesolimbic pathway from midbrain to limbic system
• Nigrostriatal pathway from substantia nigra to striatum in the
limbic system
• Involved in motor control, dopamine levels are low in Parkinson disease
• Involved in reward behavior and addiction and in psychiatric disorders
such as schizophrenia
• Receptors (metabotropic)
• D1, D2, D3, D4 D5
• D1-like (D1 and D5) increases cAMP and D2-like (D2, D3 and D4)
decreases cAMP
• Overstimulation of D2 receptors may lead to schizophrenia
• Reuptake by dopamine transporter
• Drug addiction is due to increased dopamine levels
• Cocaine and methamphetamine act by inhibiting dopamine transporters and
thereby increasing dopamine level in the brain to a unimaginably high
levels ,
• Opioids and heroin act directly on DA neurons or inhibit GABA inhibition
of DA neurons
• Cannabis and marijuana activate endocannabinoids which act
presynaptically , inhibit GABA, increases DA levels
52. Serotonin
• Chemically: 5Hydroxy tryptamine (5HT)
• present in high concentration in platelets and in the GIT, within the brain stem
in the midline raphé nuclei, which project to a wide area of the CNS including the
hypothalamus, limbic system, neocortex, cerebellum and spinal cord
• After secretion, reuptake by serotonin transporter (SERT)
• Once inside the presynaptic terminal it is metabolised by MAO
• Receptors
• Metabotropic : 5HT1 (A,B,D,E,F), 5HT2 (A,B,C), 5HT4, 5HT5 (A,B), 5HT6, 5HT7
• Ionotropic : 5HT3
• Regulate arousal, mood and social behavior, appetite and digestion, sleep, memory,
and sexual desire
• Low levels are known to be involved in depression
• Selective serotonin reuptake inhibitors – SSRI (fluoxetine, citalopram) blocks
serotonin transporter and increases serotonin levels or SNRI (Serotonin
Norepinephrine reuptake inhibitors) are also used
• Serotonin is involved in migraine (serotonin agonists are used), 5HT1 B,D,F
receptors are stimulated by antimigraine drug sumatriptan
• Serotonin antagonists are useful in vomiting
• Tricyclic antidepressants (TCAs) inhibit the reuptake of norepinephrine &
serotonin
• 5HT1A acts as autoreceptor
• 5-HT2A receptor has been implicated in the cognitive process of working memory.
Useful in schizophrenia
53. Norepinephrine
• present in the autonomic nerves, brain stem, hypothalamus,
locus ceruleus of the pons
• NE transporter is the NE reuptake pump located on
the presynaptic noradrenergic nerve terminal
• Metabolised by MAO (monoamine oxidase); MAO inhibitors are used
as antidepressants
• Increases BP and HR
• send nerve fibres to widespread areas of the brain and help
control the overall activity of the brain and the mood.
• Mostly it causes excitation but sometimes inhibition also
happens
• regulate mood, arousal, cognition, pain and other functions
• Receptors: α1A, α1B, α1D, α2A, α2B, α2C, 1, 2, 3
• Metabotropic receptors G protein coupled, second
messenger: cAMP or Ca2+ and protein kinase
• with norepinephrine having a greater affinity for α-
adrenoceptors and epinephrine for β-adrenoceptors
• Locus ceruleus is the principal site of norepinephrine in the
brain, involved in arousal, stress reaction, attention, sleep-
wake cycle
• beta1 (heart), beta2 (bronchial muscles, blood vessels), beta3
54. Opioid Peptides
• Peptides originally known to be similar to morphine
• Different types of
• Endorphin: present in pituitary, earliest discovered
opioid peptide
• enkephalins: met-enkephalin, leu-enkephalin: present at
substantia gelatinosa in the spinal cord & brain stem
reticular nuclei, widely distributed
• Dynorphin: recently discovered
• Opioid peptides are involved in the descending pain inhibitory
pathway
• receptors: , , : metabotropic, GPCR
• Activation of μ receptors increases K+ conductance,
hyperpolarizing central neurons and primary afferents.
Activation of κ receptors and δ receptors closes Ca2+ channels
• Dynorphin
• Nociceptin
• Similar to dynorphin A, bind to nociceptin receotor
• Kyotorphin
55. Glycine
• An inhibitory neurotransmitter in
the spinal cord
• It is also known to be present in
retina
• Co-activates NMDA receptor with
gulutamate
• It has ionotropic receptor:
Activate Cl- channels and cause
hyperpolarisation
• Action of glycine is antagonised
by strychnine
• Strychnine poisoning causes
56. Endocannabinoids
• The endocannabinoid system (ECS) is a widespread
neuromodulatory system that plays important
roles in central nervous system (CNS)
development, synaptic plasticity, and the
response to endogenous and environmental insults
• The ECS is comprised of cannabinoid receptors,
endogenous cannabinoids (endocannabinoids), and
the enzymes responsible for the synthesis and
degradation of the endocannabinoids
• Endogenous cannabinoids are 2-AG (2-arachidonoyl
glycerol) and anandamide (arachidonoyl
ethanolamide)
• The most abundant cannabinoid receptor is the
CB1 cannabinoid receptor, however CB2
cannabinoid receptor is also described
• Postsynaptic neuron releases endocannabinoids
which then bind to cannabinoid receptors on the
presynaptic terminal via in retrograde
transmission
• Exogenous cannabinoids, such as
tetrahydrocannabinol (Cannabis), produce their
Retrograde
transmission
57. Histamine
• present in pathways from hypothalamus to cortical areas & spinal cord
• receptors: H1, H2, H3 (all present in brain)
• functions related to arousal, sexual behaviour, drinking, pain
• H1 receptors:
• Apart from periphery these receptors are distributed in the thalamus, cortex, and
cerebellum. H1 receptor is the mediator of allergy, sedation and weight gain produced
by a number of antipsychotic and antidepressant drugs.
• H2 receptors:
• Apart from periphery, H2 receptors are widely expressed in the neocortex, hippocampus,
amygdala, and striatum and produces excitatory effects in neurons of the hippocampal
formation and thalamus. Several studies indicates that the stimulation of
these receptors produces antinociceptive effects.
• H3 receptors:
• These are located presynaptically on axon terminals. Those located on histaminergic
terminals act as autoreceptors. In addition, H3 receptors are located on
nonhistaminergic nerve terminals, where they act as heteroreceptors to inhibit the
release of a variety of neurotransmitters - including norepinephrine,
dopamine,acetylcholine, and serotonin. Particularly high levels of H3 receptor binding
are found in the frontal cortex, striatum,amygdaloid complex, and substantia nigra.
Antagonists of H3 receptors have been proposed to have appetite suppressant,arousing,
and cognitive-enhancing properties.
58. Neurokinins
• Substance P
• Neurokinin A and B
• found in primary nerve ending in the spinal cord
• mediator of pain in the spinal cord
59. Nitric oxide (NO)
• is a neurotransmitter in the central, peripheral, and
enteric nervous systems
• Inhibitory (smooth muscle relaxation)
• It has a role in a variety of neuronal functions
including learning and memory processes, cortical
arousal, nociception, food intake, penile erection,
yawning, blood vessel dilatation and immune response
• Neurons synthesize NO as a response to the activation of
N-methyl-D-aspartate (NMDA) receptors by the excitatory
amino acid glutamate
• NO is generated in the neuronal cells by the enzyme
nitric oxide synthase (NOS) with calcium and calmodulin
as cofactors
• NO has been described as an unconventional
neurotransmitter, because it is not stored in synaptic
60. Adenosine
• G protein coupled receptors
• A1, A2A, A2B, A3
• Widely distributed
• Is a neuromodulator
• Sleep promoting substance
• A1 receptors inhibits the release of
glutamate, Ach, noradrenaline, serotonin,
dopamine
• A2 receptors facilitate GABA release
• Modulate neuronal excitability, synaptic
plasticity, coordination of neural
networks and in ischemia
• Caffeine
61. Others
• CART (cocaine and amphetamine regulated transcript)
• hypothalamus and midbrain enriched neurotransmitter with an antioxidant property
• can be found in mitochondria, which is the main source of reactive oxygen species
• Systemic administration of CART has been found to ameliorate dopaminergic neuronal loss and
improve motor functions in PD
• It is a potential neurotrophic factor and is involved in the regulation of hypothalamic-
pituitary-adrenal axis and stress response as well as in energy homeostasis. CART is also
highly expressed in limbic system
• Possess antidepressant properties
• Neuropeptide Y
• influences many physiological processes, including cortical excitability, stress response,
food intake, circadian rhythms, and cardiovascular function
• increases eating and promotes obesity
• Neuropeptide Y inhibits orexin
• Leptin inhibits neuropeptide Y
• Orexin (hypocretin)
• Involved in arousal, wakefulness, and appetite
• Narcolepsy is caused by a lack of orexin in the brain due to the destruction of the cells
that produce it
• CGRP (Calcitonin gene related polypeptide)
• Present in the pain pathway at the first synapse, involved in causing
headache in migraine, CGRP antagonists which are monoclonal antibodies are
62. Different types of nerve conduction
• Sensory conduction
• Motor conduction
• Mixed neve conduction
63. Different types of nerve conduction
• Orthodromic conduction
• Antidromic conduction
• In an orthodromic study, the
recording electrodes measure the
action potential traveling in the
physiologic direction.
• In an antidromic study, the recording
electrodes measure the action
potential traveling opposite the
physiologic direction.
64. Mixed nerve
• A nerve comprised of large
number of bundles of nerve
fibres
• When a nerve is electrically
stimulated compound action
potential is generated
• This can be recorded using
surface electrodes kept on the
skin surface overlying the
nerve
65. Conduction Velocity
• If the distance form the
stimulating electrode
(cathode) to the recording
electrode (cathode) is known
the conduction velocity can be
calculated in m/s
distance
Velocity = -----------------
----------
time
•
Sensory conduction velocity
and motor conduction velocity
can be calculated
• Conduction velocity is
66. Describe Alteration in nerve
conduction in nerve injuries.
• Nerve injury causes
• Demyelination
• Nerve conduction velocity is slow down
• Axonal degeneration
• Amplitude of compound action potential is reduced
