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and to communicate with each other and with other types of cells like muscle cells. conduct impulses. .INTRODUCTION: The human nervous system consists of billions of nerve cells plus supporting cells. Among these neurons are those which are able to respond to stimuli .

COMPONENTS OF NERVOUS SYSTEM Nervous system Central nervous system Peripheral nervous system Autonomic nervous system Somatic nervous system Brain Spinal cord Sympathetic division Parasympathetic division .

CELLS OF NERVOUS SYSTEM: 1. NEURON Structural and functional unit of nervous system 2. NEUROGLIA Supporting cell of the nervous system .

NEURON  Structural and functional unit of nervous system  100 billion neurons are present in Human nervous system  Both electrically active and excitable .



Each neuron is made up of three parts:
a) Nerve cell body b) Dendrite

c) Axon

 Soma or parykaryon  Irregular shape

 Single large centrally placed nucleus.
 Nissl bodies and neurofibrils

Nissl  Tigroid substance  Small basophilic Membranous granule  Protein synthesis.  Absent in axon hillock  Flow into the dendrite but not into axon NEUROFIBRILS:  Thread like structures  Microfilaments and microtubules .NISSL BODIES: Named after the discoverer F.

one or more in number.DENDRITE  Branched shorter process of neuron  May be absent.  Conductive in nature ( DECREMENTAL CONDUCTION) .

AXON  Longer process of nerve cell  One per neuron  Arise from axon hillock  First portion of axon : Initial segment .

Internal structure of axon Long central core called axis cylinder covered by neurolemma  Axis cylinder = Axoplasm+ Axolemma  Can be myelinated or non-myelinated  Nodes of ranvier • Periodic constrictions ( Myelin is absent) • Internode • Faster conduction .

 Supporting cell of the nervos system

 10-50 times than neuroms
 Present in both CNS and PNS

1. ASTROCYTES  Star shaped  Present throughout the brain  Two types Fibrous (white matter) & Protoplasmic (Gray matter)

 FunctionForms blood brain barrier Supporting network Maintain appropriate concentration of ions and neurotransmitters.

2. MICROGLIA (MACROPHAGES OF CNS)  Smallest  Scavanger cell  Derived from monocytes

3. OLIGODENDROCYTES  Short with few process.  Myelin sheath formation (multiple fibre)

Satellite cells:  Provide support to neuron.  Regulate chemical environment of ECF around neuron .NEUROGLIA IN PNS: 1. SCHWANN CELLS:  Major glial cell in PNS  Function:  Myelination: Single neuron  Nerve regeneration 2.


On the basis of structure: Myelinated & Non myelinated 2. On the basis of neurotransmitter secreted: Adrenergic & Cholinergic .CLASSIFICATION OF NERVE FIBRES: There are various classification: 1. On the basis of function: Sensory & Motor 5. On the basis of distribution:  Somatic & Visceral/autonomic 3. On the basis of origin: Cranial & Spinal 4.

post ganglionic sympathetic .05 Afferents for pain. On the basis of diameter and conduction speed: (Erlanger & Grasser classification) CLASS OF NERVE FIBER Aα Aβ Aγ Aδ B DIAMETER OF FIBER VELOCITY OF IDENTITY OF NERVES /THIN OR THICK(MU) CONDUCTION (M/SEC) 12-22 12-6 6-3 5-2 Less than 2 120-70 70-30 30-15 30-12 10-3 Motor & proprioceptive Afferents for touch Motor for intrafusal muscle fibers of the spindle Afferents for thermal senses Preganglion fibers of the autonomic system C 1.6.3 2-.5-0.

annulo-spiral ending Golgi tendon organ FIBRE TYPE Aα Aα II III Muscle spindle. pressure Pain and cold receptors. Sensory nerve classification (Classification used by sensory physiologist): NUMBER Ia Ib ORIGIN Muscle spindle. touch. Some touch receptors Aβ Aδ IV Pain. temperature. flower-spray ending.7. and other receptors Dorsal root C .


soma or axon of another neuron) .SYNAPSE : Junction where presynaptic cell (axon or some portion of one cell) terminate on postsynaptic cell (dendrite.

Semaphorin protein & Neurolignin protein : Moderate actual synapse formation .  Guided by attractant and repellant secreted by glial cell.Growth cones :  Present at the growing tip  Right synaptic connections.

CLASSIFICATION:  Anatomical classification  Axo-axonic synapse  Axo-dendritic synapse  Axo-somatic synapse .

Chemical synapse .FUNCTIONAL CLASSIFICATION- 1. Electrical synapse 2.

ELECTRICAL SYNAPSE: Physiologic continuity between Pre & Postsynaptic neuron because of GAP JUNCTIONS .

.  Transmission in either direction.ELECTRICAL SYNAPSE: Gap junction form low resistance bridges through which ions pass with relative ease. Synaptic delay is less.

CHEMICAL SYNAPSE:  More commonly seen  Presyaptic terminal is separated from Postsynaptic terminal by a space called Synaptic cleft (20-40 nm) .

ANATOMY OF CHEMICAL SYNAPSE: PRESYNAPTIC AXON TERMINAL: Branches of axon of presynaptic neuron. . Various types:  Round or oval knobs •Terminal buttons •Synaptic knob •End-feet •Axon telodendria.

present on dendrite in cerebral and cerebellum cortex.Sometimes form a basket around postsynaptic cell in cerebellum & autonomic ganglia Wavy or coiled with free endings without the knob : -inhibitory function Each neuron divide to form 2000 synapse .Dendrite spines . Basket cells.

dense core: Catecholamines 3. Small. Large. GABA or glutamate. glycine.clear: Acetylcholine. Covered by presynaptic membrane which contain synaptic vesicles:  Types of synaptic vesicle: 1. Small. 2.dense core: Neuropeptides .

seminar\Neural Synapse.RECYCLING OF VESICLES Small vesicles gets recycled after use Regulated by V-snare protein Synaptobrevin : Vesicle membrane T-share protein Syntaxin : Neuron membrane.flv .

ANATOMY OF CHEMICAL SYNAPSE: POSTSYNAPTIC AXON TERMINAL: Covered by postsynaptic membrane Contain large number of receptor protein molecule These molecule has two components: .

Receptor molecule Binding component Bind to neurotransmitter Ionophor component Passes neurotransmitter inside the postsynaptic axon Ion channel Second messenger .

.ION CHANNEL: Allow passage of specific ion through the membrane. K and Ca Anion channel: Lined by positive ions Allow passage of anions like Cl. Rapid action Two type: Cation channel:  Lined by negative ions  Allow passage of cations like Na.

beta and gamma. .“SECOND MESSENGER” system: Prolonged affect G-Protein (Most common ) Have 3 component: alpha.

.EFFECTS OF ACTIVATOR α COMPONENT Opening of specific ion channels Activation of cAMP or cGMP Activation of some intracellular enzyme Activation of gene transcription.

CONJOINT SYNAPSE: Have both Electrical and Chemical synapse propeties .POST SYNAPTIC DENSITY: Ordered complex of Specific receptors. & Enzymes induced by postsynaptic effect. Binding proteins. SYNAPTIC CLEFT : Space between Pre & Postsynaptic neuron 200-400 angstroms wide Contain cholinesterase.

FUNCTIONS OF SYNAPSE: To transmit the impulse from one neuron to another neuron or muscle. Both excitatory and inhibitory action .

Clinical significance of EPSP:  If strong enough. Reaches peak 1-1.EXCITATORY FUNCTIONEPSP ( EXCITATORY POST SYNAPTIC POTENTIAL): Graded potential Initial depolarizing response. EPSP produced by all the active knob summate. can produce action potential .5 Ms after afferent impulse enters. Increases excitability of neuron Confined to only synapse. then declines exponentially.5 ms later. Begin 0.

Arrival of Action potential in Axon terminal Opening of calcium channels Influx of calcium ions Opening of vesicles and release of Ach Passage of Ach through synaptic cleft Formation of Ach-Receptor complex Opening of sodium channels Development of EPSP Opening of sodium in initial segment of axon Development of action potential Spread of action potential .

INHIBITORY FUNCTION: Three types : Post synaptic / Direct inhibition Pre synaptic / Direct Inhibition Renshaw cell inhibition .

glycine Mechanism of action: Causes development of IPSP( Inhibitory Postsynaptic Potential) Transmitter-receptor complex formation Opening of ligand gated K & Cl channel instead of Na channel Hyperpolarization Inhibit synapse transmission. IPSP( Inhibitory Postsynaptic Potential) .POSTSYNAPTIC INHIBITION: Due to release of an inhibitory neurotransmitter. Ex: GABA. Dopamine.

PRE SYNAPTIC INHIBITION/INDIRECT INHIBITION. Sends inhibitory impulse to motor neuron. Collateral fibre : Some of the fibre terminate on renshaw cell instead of leaving spinal cord. .  Failure of presynaptic axon terminal to release the excitatory neurotransmitter substance RENSHAW CELL INHIBITION: Renshaw are small motor neuron present in anterior gray horn of spinal cord.

SLOW POSTSYNAPTIC POTENTIALS:  Slow EPSP (due to decrease in K+ concentration) IPSP (due to increase in K+ concentration)  Seen in autonomic ganglia. cardiac and smooth muscle and cortical neurons.  Latency period : 100-500 ms and last several seconds .

 Prevented by one way gate at synapse as chemical mediators are present only in presynaptic nerve terminal .PROPERTIES OF SYNAPSE: ONE WAY CONDUCTION: Impulse are transmitted only in 1 direction in chemical synapse (BELL-MAGENDIE LAW) An impulse conducted antidromically  Dies out after at cell body of neuron.

.5 ms Clinical significance:  Helps to find out if the reflex pathway is monosynaptic or polysynaptic.SYNAPTIC DELAY: Occur during the transmission of impulse through the synapse. Occur due to time taken for Release of neurotransmitter Passage of neurotransmitter Action of neurotransmitter on receptor Action of receptor Inward diffusion of Na  Normal duration : 0.3-0.

FATIGUE: Occurs during continous activity Occurs due to exhaustion or partial exhaustion of neurotransmitter store Destroyed by acetylcholinesterase New acetylcholine is not synthesized Progressive inactivation of receptor Slow development of abnormal concentration of ions inside postsynaptic neuronal cell. .

CONVERGENCE AND DIVERGENCE: Anatomic substrates for Facilitation . Divergence: One presynaptic neuron terminate on many postsynaptic neuron. ConvergenceMany presynaptic neurons terminate on a single postsynaptic neuron. Occlusion and Reverberation. Can be amplifying type or the one diverging into multiple tracts. . Can be from single or multiple source.

Temporal summation: One nerve fibre stimulated repeatedly . Spatial summation: Many presynaptic terminals are stimulated simultaneously 2.SUMMATION :  Fusion of effects of progressive increase in the EPSP leading to facilitation of response. 1. It is of two types.

and larger molecule 1.  Ex:Transmission of sensory signals . Small molecule:  Rapidly acting transmitters:  Causes acute response of nervous system.NEUROTRANMITTERS: More than 50 types have been reported Two types-Small molecule.

Acetylcholine Class II.Amines (Norepinephrine. . epinephrine dopamine. serotonin.000 acetylcholine molecule Continuously recycled. Glycine.histamine) Class III-Aminoacids ( GABA.2000 to 10. Aspartate) Class IV-Nitric oxide(NO) Synthesized in cytosol of presynaptic terminal Absorbed by active transport into the Synaptic vesicles  1 vesicle contain .TYPES: Class I. Glutamate..

slowly acting transmitters: These are neuropeptide  Ribosomes.2. Two changes occur in golgi bodies:  Split enzymatically  Packaged into minute transmitter vesicles  Released into cytoplasm  Axoplasmic streaming  More potent  Prolonged actions . Large molecule.

EXCITABILITY:  Nerve fibre have low threshold than other cells. Two types of response :  Action potential / Nerve impulse  Electrotonic potential / Local response / Graded potential . CONDUCTIVITY 1. EXCITABILITY 2.PROPERTIES OF NERVE FIBRE: 1.

IONIC BASIS OF ELECTRICAL EVENTS: RESTING MEMBRANE POTENTIAL  -70 mV.  Maintained mainly by :  Sodium Potassium pump:  Selective permeability of membrane  Leak channels .

.  First node of ranvier.SODIUM POTASSIUM PUMP  Na and K are actively transported in opposite direction  3 Na out and 2 K in  Uses energy from ATP  Highly concentrated in :  Initial segment.  Sensory neurons.

flv . seminar\Resting Membrane Potential.SELECTIVE PERMEABILITY OF MEMBRANE: Depend on gated channels Only specific ion can pass through LEAK CHANNELS: Na and K both ion can diffuse back by leak channels.

 Begins in initial segment of the axon  Recorded using Electronic amplifier & Cathode ray oscilloscope (CRO).ACTION POTENTIAL:  Series of electrical events that occur in nerve membrane when nerve fibre is activated  Rapid & Small changes  Occur in two phases – Depoarization and repolarization  Studied in motor neuron and anterior horn of spinal cord. .

 Following action potential curve is obtained. .

1. STIMULUS ARTIFACT:  Slight irregular deflection of baseline  Last for a very short period of time.  Last for 0.  Leakage of current from stimulated electrode to recording electode. 2. LATENT PERIOD:  Isopotential interval  Follows stimulus artifact  Ends with the start of action potential  Time taken : site of stimulation to recording electode.5-1 ms .

3. then shoots up beyond it till +35 mV . then increases suddenly  Firing level : Point at which the depolarization increases suddenly 4. OVERSHOOT: From firing level curve reaches isoelectric potential rapidly . FIRING LEVEL:  Depolarization starts after latent period  Very slow for about 15mv.

5. REPOLARIZATION:  Starts when depolarization is completed  Initially it is rapid later it become slow 6. SPIKE POTENTIAL:  Rapid rise in depolarization and rapid fall in repolarization  Rate of repolarization decreases when it is almost 70 % completed.  Last for 0.4 ms .

7. Last for 2-4 mS 8. AFTER DEPOLARIZATION / Slow repolarization NEGATIVE AFTER POTENTIAL: Follows rapid fall in repolarization. it becomes more negative beyond resting level. changes in Afterpolarization may occur without changes in the rest of the action potential. . Last for 40 Ms  On repeated conduction. AFTER HYPERPOLARIZATION / POSITIVE AFTER POTENTIAL: After reaching the resting level.

MONOPHASIC ACTION POTENTIAL: Electric potential recorded with one electrode on surface & one inside the nerve fibre. BIPHASIC ACTION POTENTIAL: Both electrode on surface .

flv  Onset of depolarization : Slow influx of Na  Spike potential : Rapid opening & rapid closing of voltage gated Na channel  Repolarization : K channel start opening  Hyperpolarization : K channel remain open for long time .ACTION POTENTIAL (ionic basis) seminar\Action Potenital.

GRADED POTENTIAL:  Mild local change in membrane potential when stimulated.  Develop in  Receptor  Synapse  Neuromuscular junction .

.  Constant amplitude and velocity.2. CONDUCTIVITY:  Transmiting the impulse from area of stimulation to the other tissue.  Unidirectional  In experimental condition : Either direction.

Myelinated fibre :    50 times faster Because of saltatory conduction ( depolarization jumps from one node to another node) seminar\Action potential propagation in an unmyelinated axon.flv .flv seminar\Saltatory Conduction.

Absolute refractory period:  Nerve doesnot show any response at all 2. . Two types- 1. if strength of stimulus is increased to maximum.REFRACTORY PERIOD Period at which nerve doesnot give response to a stimulus. Relative refractory period:  Nerve fibre shows response .

ADAPTATION:  Also called desensitization  Decline in discharge of sensory impulses when receptor is stimulated continuously  Partial or complete. Two types: Tonic and Phasic .

Phasic /Rate/Movement receptors Rapidly adapting receptors  Detect change in stimulus strength  Ex:Touch and pressure receptors . 2. Tonic receptors Slowly adapting receptors  Detect continous stimulus strength  Ex: Musle spindle.1. Pain and Chemoreceptors.

ALL OR NONE LAW: When a nerve is stimulated by a stimulus either it gives maximum response or doesnot give response at all. .

COMPARISON OF ACTION POTENTIAL AND GRADED POTENTIAL ACTION POTENTIAL Propagative Long distance signal Both depolarization and repolarization Obey all or none law Summation not possible Has refractory period GRADED POTENTIAL Non-propagative Short distance signal Only depolarization and hyperpolarization Does not obey Possible No refractory period .

TRANSMISSION AND PROCESSING OF SIGNALS IN NEURONAL POOL NEURONAL POOL: Collection of few or vast number of neurons. STIMULATORY FIELD : Neuronal area stimulated by a nerve fibre. EXCITATORY / SUPRATHRESHOLD STIMULUS: Stimulus which causes a neuron to discharge SUBTHRESHOLD STIMULUS : Stimulus itself doesnot cause a neuron to discharge Make neuron more susceptible to other incoming signal .

ZONES OF A NEURONAL POOL:  Discharge/excited/liminal zone: in centre  Facilitated/subthreshold or subliminal zone:  Present around the discharge zone.  Inhibitory zone AFTERDISCHARGE  Prolongation of a signal by a neuronal pool.  Can occur due to:  Long acting synaptic transmitter  Reverberatory (oscillatory circuit) .

REVERBERATORY (OSCILLATORY CIRCUIT): Caused by positive feedback Can involve single neuron with a collateral nerve or many parallel fibres  Fatigue .

Ex: Walking movement. RHYTHMICAL SIGNAL OUTPUT  Result from reverberating circuit or sequential reverberating circuits.  Reverberatory circuit.CONTINOUS SIGNAL OUTPUT Occur because of:  Continous intrinsic neuronal excitability. respiratory signal .

RECEPTORS  Sensory nerve endings terminate in the periphery as bare unmyelinated endings or in specialized capsulated structures.  Act like a transducer .  Five Types : a) Mechanoreceptor b) Thermo receptor c) Nociceptor d) Electromagnetic receptor e) Chemoreceptor .convert Stimuli into Action potential.

. WEBER FECHNER LAW:  Change in response of a receptor is directly proportional to logarithmic increase in intensity of stimulus.PROPERTIES OF RECEPTORS: SPECIFICITY OF RESPONSE Also called doctrine of specific nerve energie/ Muller’s law  This specificity of nerve fibre for transmitting only one modality of sensation is called the labeled line principle.

RECEPTOR POTENTIAL: Studies in pacinian corpuscles It is a nonpropagated potential Develop when a receptor is stimulated Maximum amplitude reached is 100 mV Amplitude increases rapidly first then progressively slowly Frequency increases in proportion to receptor potential .

Pressure stimulus Compression & elongation of pacinian corpuscle SEQUENCE OF EVENTS IN DEVELOPMENT OF RECEPTOR POTENTIAL Deformation of centre core fibre Opening of mechanically gated Na channel Na ions into the core fibre Receptor potential LOCAL CIRCUIT Spread of local circuit to first node of ranvier Opening of voltage gated Na channel Generation of Action potential .

Can derive from :  Organ they innervate  Schwann  Astrocyte  Cell or the nerve itself  Can undergo anterograde or retrograde transport . survival and growth of neuron.FACTORS AFFECTING NEURONAL GROWTH: NEUROTROPHINS : Proteins necessary for Development.

FOUR ESTABLISHED NEUROTROPHINS AND THEIR RECEPTORS ARE: NEUROTROPHIN RECEPTOR Nerve growth factor ( NGF) Brain derived neurotrophic factor (BDNF) Neurotrophin 3 ( NT-3) Neurotrophin 4/5 ( NT-4/5) Trk A Trk B Trk C Trk B p75 NTR : One low affinity NGF receptor. .

OTHER FACTORS AFFECTING NEURONAL GROWTH CNTF ( ciliary neurotrophic factor) : GDNF (glial cell derived neurotrophic factor) LIF (leukemia growth factor) IGF-I (insulin like growth factor I) TGF (transforming growth factor) FGF (fibroblast growth factor) PDGF (platelet derived growth factor) .

CLINICAL SIGNIFICANCE OF SYNAPTIC INHIBITION: Poison like strychnine block inhibitory function Tonic muscle spasm Parkinsonism : inhibitory system is impaired Rigidity .APPLIED SCIENCE : 1.

FEW TOXIN EXERT THEIR ACTION BY BLOCKING NEUROTRANSMITTER RELEASE: Tetanus toxin: Block Presynaptic transmitter release in CNS spastic paralysis Botulinum toxin : Block release of acetylcholine Flaccid paralysis  Local injection are used In facial muscles to remove wrinkles .2.

THEOPHYLLINE AND THEOBROMINE Reduces threshold. Ex: multiple sclerosis 4. Increases neuronal excitability . CAFFEINE.3. LOSS OF MYELIN Delayed or blocked conduction.

EFFECT OF ALKALOSIS AND ACIDOSIS Alkalosis increased neuronal excitability Ex: overbreathing precipitate epileptic attack. . Acidosis decreases neuronal excitability: Ex: Coma in diabetic or uremic acidosis 6. EFFECT OF PRESSURE: Loss of conduction in large fibre Small pain fibres not effected Ex: Saturday night or Sunday morning paralysis.5.

Occur during the depolarization phase of the action potential.  Many theories have been proposed to explain the mechanism of action of local anesthetics. Acetylcholine theory Surface charge theory Membrane expansion theory Calcium displacement theory Specific receptor theory (Most accepted theory) . EFFECT OF LOCAL ANAESTHESIA: Exert their effect at nerve membrane.7.

Displacement of calcium ion from the sodium channel receptors site Binding of the local anesthetic molecule to "this receptor site Blockade of the sodium channel Decrease in sodium conductance Depression of the rate of electrical depolarization Failure to achieve the threshold potential level Lack of development of propagated action potential Conduction blockade Seminar \ lidocaine in action 2.flv .


Inadequate pulpal anesthesia develop sometime in the presence of subjective symptoms of adequate soft tissue anesthesia Cutaneous afferents are smaller than pulp afferents and thus more susceptible to the local anesthetic.FEW CLINICAL ASPECTS OF LOCAL ANAESTHESIA 1. Even in case of excellent pain control patient sometimes feel pressure because  Mechanoreceptors pain fibres are relatively large and frequently not affected by anaesthetic  Group C pain fibre are effected before group A touch Fibre . 2.

Recovery is usually a slower process than induction because the local anesthetic is bound to the drug receptor site in the Na channel and hence released more slowly than it is absorbed.3. EFFECT OF LIPID SOLUBILITY Increasing lipid solubility Faster nerve penetration Rapid action. 5. . Molars are anesthetized much earlier than the incisors because fibers near the surface of the nerve innervate more proximal regions.whereas fibers in the core bundles innervate the more distal points of nerve distribution 4.

EFFECT OF INFLAMMATION Reduced affect seen because of :  Increased ionised form  Some inflammatory exudate lowers the response threshold  Dialated vessels : Rapid uptake of anaesthetic molecule .6.

ALTERNATIVE :  Inject in a distant site  Inject large amount of anaesthetic  Histamine blockers as anaesthetic  General anaesthesia  Alternative method of pain control:  Electronic Dental Anaesthesia (TENS)  Hypnosis .

. AND SOMAN) Developed by Germany during as a weapon of chemical warfare during World war II but not used VX  Produced in huge quantities by the U.  stockpiling and use during war are now banned by the Chemical Weapons Convention of 1993.S & Soviet union during the Cold War of 1993.NERVE GAS: ORGANOPHOSPHORUS COMPOUNDS (TABUN. SARIN.

can be absorbed into the bloodstream and paralyze the nervous system. Affects the transmission of nerve impulses through the nervous system. if inhaled or in contact with the skin. leading to respiratory failure and immediate death . A single droplet of VX or Sarin.


especially the ability of electrical conduction.  Normal conduction velocity is 50 to 60 mps (approx)  Related to the diameter of nerve and myelination . Nerve conduction velocity (NCV) :  Common measurement made during this test.NERVE CONDUCTION STUDY (NCS) Nerve conduction study (NCS) :  A test commonly used to evaluate the function. of the motor and sensory nerves of the human body.

Patch-like 2 electrodes are affixed on the skin at various nerve locations. Speed of the Recorded on a moitor . A probe emits a very low electrical impulse.PROCEDURE: Patient may lie down or sit during the test.

 Myopathy. weakness.  Diagnose Focal neuropathy (carpal tunnel syndrome). Differentiation between local or diffuse disease process Prognosis of nerve injury. - .  Symptoms indicative of nerve damage as numbness.  Diagnose Peripheral neuropathy.  Diseases of neuromuscular junction ( mythenia gravis).USES OF NCS  Localize site of pain  Nerve damage from herniated discs.

Slowing of all nerve conductions . or generalized peripheral neuropathy. Example: Carpal tunnel syndrome: Focal compression of median nerve at wrist Slowing across the wrist for the motor and sensory latencies Generalized diseased of nerves.INTERPRETATION OF NCS:  Slowing of the NCV indicates there is damage to the myelin.

Hence to better understand the mastermind behind all the activities carried out by the complex body. . physiology and clinical implications. it is must to have a firm knowledge of its structure. which control all the other systems of the body.CONCLUSION: Neuron are the electrically active and excitable cells forming the building blocks of a system.

5th edition  Monheim’s Local anesthetic and pain control.Handbook of local anaesthesia.Review of medical physiology 21st edition  K. .Sembulingam-Essentials of Medical Physiology.REFERENCES  Guyton -Textbook of medical physiology--11th edition  William F Ganong .  Malamed.