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Peculiarities of a neuron

Axon hillock: The thickened area of cell body from which axon arises
Initial segment: The first 50 to 100 m of the axon.
Axon telodendria: Also called synaptic knobs or terminal buttons

  1. Nissl substance (also called Nissl bodies or granules) This is composed of large aggregations of rough endoplasmic reticulum. The Nissl substance extends into the dendrites but is absent in axon hillock and axon.
  2. Neurofibrils: These represent the microfilaments and microtubules of other cells of the body.
  3. No centrioles

Myelin formation

i. In peripheral nerves: By schwann cells. Schwann cell forms myelin on one axon
ii. In CNS: By oligo dendro gliocytes. Oligodendrogliocyte from myelin on many axon



Myelin is absent at
i- Nodes of Ranvier                           
ii- Axonal endings
iii- Soma                                                             
iv- Initial segment

Position of cell body

  1. It is often at the dendritic zone end of axon
  2. Sometimes, it is within the axon eg. auditory nerve
  3. Sometime, it is attached to the side of the axon eg. cutaneous nerve

Functional Areas of Neuron



Generation of action potentials

The Axon Hillock in spinal motor neuron (More Na+ Channels & proximal to cell bady so summation here)

The initial node of Ranvier in cutaneous sensory neurons(same mechanism)

Transmission of action potential

Axonal process

Release of synaptic transmitter

Nerve endings

Axoplasmic Transport


I. Fast (20-400mm/day) use molecular motors which run on Microtubule filaments


II. Slow (0.2-0.4mm/day) by microtubules and neurofilaments themselves

1. Anterograde

By kinesin

Transport of mitochondria, reticulum, small vesicles etc.

This is always anterograde

Transport of soluble enzymes, tubulins of microtubules etc

2. Retrograde

By Dyenin

Transport of proteins, small molecules, also virus, toxins like tetanus toxin



Nerve degeneration/regeneration


Nerve Degeneration

Nerve regeneration

  1. Anterograde (Wallerian)
  • Axoplasm breaks down
  • Myelin breaks down
  1. Anterograde
  • Macrophage eating away the debris, leaving an empty endoneureal tube.
  • Schwann cell regeneration
  • Axonal sprouting
  1. Cell Body
  • Chromotolysis (Nissl bodies break down - 1st change in cell body)
  • Cell swelling
  • Nucleus move to periphery
  1. Cell Body
  • Nissl bodies and Golgi apparatus gradually reappear
  • Cell regains its normal size
  • Nucleus returns to central position


Regeneration occurs at the rate of 1mm/day or 2.5 cm/month


1. CRO (Cathode ray oscilloscope)

This is used to measure electrical events in living tissue; the advantage being that it is an inertia less, instantaneously responding lever.


2. Concept of polarity

All cells have a resting membrane potential (refer : general physiology)

If a cell with a R.M.P. of say, -70mv changes to say –60mv, the cell is said to be depolarized (note that one has to ignore the negative sign while commenting on the change of polarity)

Other illustrative examples














3. Changes seen during stimulation of a nerve

One would require a set of stimulating electrodes (S) and a set of (R) recording electrodes




The recording electrodes can be such that one electrode is on the surface and the other, inside the cell; or else, both recording electrodes can be on the surface. When both the electrodes are on the surface, a biphasic action potential is recorded.



  1. Nerve is a poor conductor of electricity
  2. Nerve can conduct impulses in both directions
  3. However, once it starts going in one direction, it cannot come back because it finds the previous part of the nerve refractory
  4. Stimulation almost always occurs at cathode


While stimulating the nerve, the following changes/ events occur


i. Electro tonic potentials

These are potential changes that occur in the nerve due to passive addition of charge; for example, at the cathodal end of the stimulating electrode, negative charge are added on the surface and at the anodal end of the stimulating electrode, positive charges are added

Illustrative examples


Therefore, electrotonic potential, can be either cat-electrotonic or an-electro tonic.


ii. Local response

Upto say –70mv to –63mv, electrotonic potentials can be seen i.e., the addition of ‘7’ negative charge at the cathode causes exactly 7mv change. However, beyond this, a further addition of ‘1’ negative charge may cause the potential to change by more than 1 eg. from –63mv, it may become –61mv. This is called the local response i.e. the change in the potential is more than what you would expect on the basis of passive addition of charge.

This shows that the membrane is now participating is the process The local response in due to opening up to some of the voltage gated sodium channels.


iii. Action potential

When the local response brings out a change of say 15mv (i.e. from –70mv to –55mv), the firing level is reached wherein a large number of voltage – gated sodium channels open up and cause the action potential   

To summarise,         


Electrotonic potential (is due to)

Passive addition of charge

Local response (is due to)

Opening up of some of the Na+ channels

Action potential (is due to)

Opening up of many Na+ channels


[Difference between Local potentials and Action potential]

Example :
Example of Local potential: EPSP/IPSP, dendritic potentials, Motor End-plate potential, receptor potential, synaptic potential, generator potential,  electrotonic potential


                Local Potential

Action potential

1. Does not follow all or none law

Follows all or none law

2. Not self – propagating

Self – propagating

3. Can summate to produce AP

No summation

4. Can be depolarizing/hyperpolarizing

Always depolarizing

5. No refractory period,

Has refractory period

Phases of an action potential            


Text Box:


Depolarization in Various Tissue Due to
1) Nerve Na+
2) Skeletal muscle Non specific cation channel
  Na+ channel
3) Smooth muscle Ca++
4) SA Node Ca++
5) Ventricular muscle Na+
6) Endolymphtics Potentials K+ influx
1 = R.M.P.
2. Cat – electrotonic potential
3. Local response
4. Firing level / threshold
5. Depolarization
6. Overshoot /Spike Potential
7. After – Depolarization
8. After – hyperpolarization

i. During after-depolarization, the excitability of nerve is more than after-hyperpolarization so most excitable part of refractory period.
ii. During after-hyperpolarization, the excitability of nerve is less, when compared to resting phase.


Refractory Period: 2 parts Absolute refractory period (ARP) & Relative refractory period(RRP) 

Absolute refractory period:no stimulus can result in 2nd AP. From above firing level depolarization to 1/3rd of repolarisation. Excitability is zero.

Relative refractory period: a strong stimuli can lead to 2nd AP. From 1/3rd of repolarization to RMP. Excitability is less. Include after-depolarization (less refractory) & after-hyperpolarization (more refractory)

Strength – Duration Curve  


1.  Rheobase

The minimum strength of current to stimulate a nerve, regardless of the time it takes

2.  Utilization time

Time taken for the rheobase current to stimulate a nerve

3.  Chronaxie

Time taken fro twice the rheobase current to stimulates a nerve

4.  Summation

2 subthreshold stimuli can summate to produce AP

Can be Spatial (2 stimuli at 2 different place) or Temporal (2 successive stimuli one after another)


Other Terms


Biphasic action potential

This type of record is obtained when both the recording electrodes are on the surface of the nerve


Compound action potential (multi peaked action potential)

Seen in a mixed nerve, wherein there may be several fibre types



Slowly rising currents fail to fire (stimulate) the nerve

Cause : The opening of K+ channels balances the gradual opening of Na+ channels

Nerve Fibre Classification    

1. Erlanger and Gasser classification

Fibre types


Fibre diameter (m)

Conduction velocity (m/s)



Proprioception; somatic motor





Touch, pressure





Motor to muscle spindles





Pain , cold, touch





Preganglionic autonomic




Dorsal root

Pain, temperature, some mechanoreceptor, reflex responses





& Parasym.

Postganglionic sympathetic



A and B are myelinated; C are unmyelinated


2. Numerical classification (for sensory neurons only)




Fibre type



Muscle spindle, annulo spiral ending

Golgi tendon organ




Muscle spindle, flower-spray ending; touch, pressure



Pain and cold receptors; some touch receptors



Pain, temperature and other receptors

Dorsal root C


Susceptibility to:

Most Susceptible


Least Susceptible









Local anesthetics






Substance p is released in response to vpain in periphery. (AIIMS Nov 09)

A. Nerve terminals              
B. Mast cells
C. Endothelium                    
D. Plasma


A. Nerve terminals


Muscle spindle function is: (AIIMS May 09)

A. Length              
B. Stretch
C. Touch                
D. Temperature


A.  Length              

Conduction of action potential or nerve impulse


Action potential




Local currents (“current sink”)

Which in turn causes



Action potential and so on

Main factor affecting conduction velocity

  1. Axon diameter : More the diameter, more the speed of conduction
  2. Myelination : Increases conduction velocity by saltatory conduction.

C.N.S. glial cells           


Formation of myelin




Induce capillaries to develop tight functions to form blood brain barrier. Also K+ uptake, Embryonal neuronal migration, NGF secretion, Metabolism of drugs, neurotransmitters etc

Muscle-Skeletal Muscle

1. Hierarchy of muscle structure


2. Cytoskeletal proteins

A. Contractile

i. Myosin (The type of myosin present in skeletal muscle is myosin II)

ii. Actin

B. Regulatory (‘or relaxing’)

i. Tropomyosin   

ii.  Troponin


ii. Titin
iii. Nebulin
iv. Dystrophin

Bands / Lines

i. Bands – A, I, H  ;  Lines – Z, M

ii.A band – Dark, made up of myosin

iii.I band – Light, made up of actin, mainly

  • H – The lighter portion of A band, where there is no overlap of actin and myosin
  • Z line – The actin filaments get anchored here; the length of the muscle between 2 Z-lines is called s sarcomere
  • M line – The central bulge in the myosin filament
  • When a muscle contracts, the two Z- lines come closer; the length of the A band remains constant whereas the length of I and H band decreases. The M – line becomes more prominent. 

Structure of Thick/thin filaments

Thick filament is made up of myosin (myosin II)

Myosin II has 2 globular heads; (Myosin I has one globular head)

The globular head has

i. actin – binding site

ii. Catalytic site for hydrolysis of ATP


3. Thin filament

  1. Is made up of actin (mainly), tropomyosin and troponin (troponin I,T,C) Other proteins: providing stability to sarcomere
  2. Desmin: Desmin is a type III intermediate filament found near the Z line in sarcomeres These connectionsmaintain the structural and mechanical integrity of the cell during contraction while also helping in force transmission and longitudinal load bearing
  3. Titin :Titin is a large abundant protein of striated muscle. A N-terminal Z-disc region and a C-terminal Mline region bind to the Z-line and M-line of the sarcomere respectively so that a single titin molecule spans half the length of a sarcomere
  4. Actinin :Actinin is a microfilament protein. a-Actinin is necessary for the attachment of actin filaments to the Z-lines in skeletal muscle cells.

Sarcotubular System  

Made up of:

  1. L-tubule (Longitudinal tubule) This is the sarcoplasmic reticulum.
  2. T – tubule (Transverse tubule) this is the invagination of the sarcolemma into the muscle cell 

The L-tubule (Sarcoplasmic reticulum) has got ‘distended ends’ called cistern

The 2 cisterns associated on either side of the T-tubule – is called a triad


a. Receptors

i. T-tubule has dihydrophyridine receptor [ (1) in the diagram above]

ii. The L tubule cistern has ryanodine receptors [(2) in the diagram above];

b. Ryanodine receptor(RyR) : Ryanodine receptors mediate the release of calcium ions from the sarcoplasmic reticulum, essential for muscle contraction. In skeletal muscle, it is thought that activation occurs via a physical coupling to the dihydropyridine receptor.

Dihydropyridine receptor : it is a voltage-dependent calcium channel found in the transverse tubule of muscles. In skeletal muscle it associates with the ryanodine receptor RyR via a mechanical linkage. It senses the voltage change caused by the end-plate potential.

Ca2+- Mg2+ ATPase : moves Ca2+ back into the reticulum, producing relaxation

Functions of the T – tubule and L –tubule


The transverse tubule is continuous with the membrane of muscle fibre. It forms a grid perforating the individual muscle fibrils. The space between the 2 layers of the T- system is an extension of the extra cellular space


ii. The T system allows rapid transmission of action potential from cell membrane to all fibres in muscle


iii. The L – tubule


iv. The L-tubule (sacroplasmic reticulum) is concerned with Ca++ movement and muscle metabolism

Excitation – contraction coupling     

The process by which depolarization of the muscle fibre initiates contraction is called excitation – contraction coupling.



1. Action potential generated in a nerve has to cause action potential in the muscle cell membrane


2. In the muscle cell membrane, depolarization normally starts at the motor end plate, the specialized stricture of the muscle cell membrane under the motor nerve ending The depolarization at the motor-end plate is called end plate potential (EPP)


3. The depolarization at motor-end plate, if large enough, causes action potential in the adjacent parts of the muscle cell membrane


4. The action potential thus generated is able to reach all the muscle fibrils in the muscle cell interior via the T-tubules


5. This triggers release of Ca++ from the terminal cisterns of the L-tubule


6. The released, Ca++ binds to troponin – C (There are 3 ‘parts’ of troponin – troponin I, T and C)(Troponin T : binds the other troponin components to tropomyosin) (Troponin I : inhibits interaction of myosin & actin) (Troponin C : has Ca++ binding sites that initiates contraction)



7. This allows he troponin to get ‘lifted off’ the tropomyosin


8. The tropomyosin ‘moves away’, uncovering the sites where myosin heads bind to actin


9.This triggers the cross-bridge cycling, including the power-stroke


10. Relaxation is brought about by the active pumping of Ca++ back into the sarcoplasmic reticulum (Note that the troponin – tropomyosin complex is the relaxing protein that inhibits the actin myosin interaction)

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