Classification of Neuron

Unipolar: They have one pole from where axon and

dendrite arise. Seen only in embryonic stage of
humans
Bipolar: Have two poles. Axon arise from one and
dendrite from the other. Commonly found in retina and
olfactory cortex
Multipolar: Have many poles. One pole gives rise to
axon and all other poles give rise to dendrites.
Commonest type of neuron
Pseudopolar: two fibres fuse at a short distance from
the cell body. E.g dorsal root ganglion. Here fibres
come from a sensory receptor and the other enters the
CNS
 Neurons can also be: Motor (carry
motor impulse from CNS to periphery
aka efferent nerves) and sensory
(carry sensory impulses from
periphery to CNS).
Another classification is : Golgi type
1 (having long axons) and Golgi type
2 (having short axons)
 Nerve Fibres Classification
Aside the earlier distribution of
neurons we can classify nerve fibres
as:
Myelinated or Non-myelinated;
Somatic or Visceral; Cranial or Spinal;
Sensory or Motor; Adrenergic or
Cholinergic; Type A or Type B or Type
C.
 Properties of Nerve Fibres
Excitability: A hallmark of nerves is
their excitability. This is defined as
the physiochemical change that
occurs in a tissue when stimulus is
applied. They can respond to
electrical, chemical or mechanical
stimuli.
Two types of physiochemical
disturbances are produced: local
nonpropagated (synaptic, generator
or electrotonic potentials-when
subliminal stimulus applied) and
 Action potential: In nerves RMP is -70mV, firing
level is -55mV, depolarization ends at =35mV.
In skeletal muscle (-90mV, -75mV and +55mV)
Conductivity:
The ability of nerve fibres to transmit the impulse
from the area of stimulation to other areas.
Normally, in the body AP, is transmitted
unidirectionally but experimentally it has been
found to travel in either direction
AP travels by depolarization of neighbouring
areas
Saltatory conduction is the form of conduction
seen in myelinated fibres which is 50times
faster than a nonmyelinated nerve
 Refractory period: Nerve fails to respond to
any stimulus: Absolute and Relative RP.
Summation:Response by 2 or more
subliminal stimuli
Adaptation: Greater excitability in the
beginning with decreasing response until no
response at all (inactivation of Na+ pump
and increase efflux of K+)
Infatigability: A nerve fibre cant be fatigued.
The reason for this is that the nerve fibre
can only conduct one AP at which time it is
refractory
All or None Law: Max response or none at all
 Degeneration and Regeneration of
Nerve Fibres
The various changes that occur in nerve fibre
when injured are termed degenerative
changes
Sunderland classified nerve injury into:
First degree injury: most common type,
caused by applied pressure over a short
period leading to hypoxia
Second Degree: aka axonotmesis due to
prolonged severe pressure resulting in
Wallerian degeneration. Intact endoneurium.
Repair takes about 18months
 Third degree: interrupted
endoneurium.epi and perineurium
are intact. Recovery is slow and
incomplete. NB:3rd 4th and 5th degrees
are called neurotmesis
Fourth degree: epineurium and
perineum are interrupted.
Regeneration poor and incomplete
Fifth degree: complete transection of
nerve trunk with loss of continuity.
Useful regeneration is not possible.
 Degenerative changes in Neuron:
Wallerian/orthograde degeneration: pathologic
changes tha t occurs at the distal cut end of
nerve axon. The observed changes are:
Swelling and breaking up of the axis cylinder
into small pieces. After few days they appear as
debris
Slow disintegration of myelin sheath into fat
droplets
Rapid multiplication of schwann cells with
invasion by macrophages removing the left
overs of the above two. This leaves behind an
empty neurilemmal tube which is later filled by
schwann cell cytoplasm
 Retrograde degeneration: pathologic
changes in a nerve cell body and axon
proximal to a cut. Changes seen in the cell
body are :
Disintegration of Nissl granules by
chromatolysis
Disintegration of golgi apparatus
Accumulation of fluid in cell body
Displacement of nucleus towards periphery
with dissapearance of neurofibrils
Extrusion of the nucleus at certain time
leading to irreversible damage
 Transneural degeneration: this is degenerative
changes that occur in the neuron with which the
cut afferent neuron synapse. E.g
Chromatolysis in cells of LGB due to cutting of
CN2
Dorsal horn cells degeneration when posterior
nerve root is cut
Degeneration of ventral horn cells when there is
a tumour in cerebral cortex
Nerve Fibre Regeneration
This is referred to as the re-growth of damaged
or lost part of a nerve tissue. It starts as early as
day 4 after injury and completed after about 80
days
 Stages of Regeneration
Extensions/pseudopodia called fibrils or
regenerative sprouts are seen prox to the cut
end
Fibrils move towards distal cut end
Some of the fibrils enter the neurilemma tube
Schwann cells line up in the neurilemma tube
guiding the fibrils into the tube
Axon cylinder is fully established inside the
neurilemma. A process completed in about 3
months from injury
Formation of myelin sheath completed in 1
year
 Gradual increase of nerve diameter
Nissl bodies and golgi apparatus appear in cell
body
Nucleus occupies centre
Functional recovery takes a long to occur after
the anatomical regeneration
Criteria for Regeneration
Gap between cut ends should be at most
3mm
Neurilemma should still be present
Intact nucleus
Alignment of the two cut ends. Any displaced
end makes regeneration not possible
 Receptors
These are sensory (afferent) nerve
endings that terminate in the periphery
as bare unmyelinated endings in the form
of specialized capsulated structures.
There are many sensory receptors that
relay information about the internal and
environment to the CNS but do not reach
consciousness
Sensory receptors can be thought of as
transducers that convert various forms of
energy into action potential
 Cutaneous Mechanoreceptors: there are
four types of mechanoreceptors that sense
pressure and touch:
Meissners corpuscles: dendrites
encapsulated in connective tissue and
respond to changes in texture and slow
vibrations
Merkel cells: expanded dendritic endings,
that respond to sustained pressure and
touch
Ruffini corpuscles: enlarged dendritic
endings with elongated capsules and they
respond to sustained pressure
Pacinian corpuscles: Consists of unmyelinated
dendritic endings of a sensory nerve.
Responds to deep pressure and fast vibration
Nociceptors:
Mechanical nociceptors: responds to strong
pressure e.g from a sharp object
Thermal nociceptors: activated by skin temp
above 42C by severe cold
Chemically sensitive nociceptors: responds to
various chemicals like bradykinin, histamine,
high acidity and irritants
Polymodal nociceptors respond to a
combination of these stumuli
 Impulses from nociceptors are transmitted via
two fibres
1.the thin myelinated A fibres which release
glutamate and is responsible for fast/epicritic
pain.
2.unmyelinated C fibres which release both
glutamate and substance P responsible for
delayed second pain aka slow/protopathic pain
There are varying number of receptors located
on the endings of nociceptive sensory nerves
that respond to noxious thermal, mechanical or
chemical stimuli. Many of these form part of a
family of nonselective cation channels called
transient receptor potential (TRP) channels
 Thermoreceptor:
Dendritic endings of A fibres and C fibres contain
innocuous cold receptors whereas on C fibres there
are innocuous warmth receptors.
There are 4-10x as many cold-sensitive as heat
sensitive spots on the skin
30C is the activation threshold of warmth receptors
and they increase their firing rate as the skin temp
increases to 46C. At 40C cold receptors are
inactive but steadily increase their firing rate as skin
temp falls to about 24C .
Further drop in skin temp leads to decrease in the
firing rate of the cold receptors until 10C below
which they are inactive and cold becomes an
effective local anaesthetic
Visceroceptors
These are situated in the viscera e.g
Stretch receptors: Heart;
Baroreceptors: Blood vessels;
Chemoreceptors:GI tract;
Osmoreceptors: Urinary tract, Brain
Sensory Modality Stimulus Receptor Receptor
system Energy class cell types
Somatosens Touch Tap,flutter Cut Meissner
ory mechRec corpc
Somatosens Touch Motion Cut Hair follicle
ory mechRec Rec
Somatosens Touch Deep Cut Pacinian
ory press,vibr mechRec corpc
Somatosens Touch Touch, Cut Merkel cells
ory pressure mechRec
Somatosens Touch Sustained Cut Ruffini corpc
ory press mechRec
Somatosens Propioceptio Stretch MechRec Muscle
ory n Spindle
Somatosens Propioceptio Tension MechRec Golgi Tend
ory n Org
Somatosens Temp Thermal ThermoRec Cold/Warm
ory Rec
Somatosens Pain Chem,Ther ChemoRec,T Chem,therm
ory m, Mech hermoRec,M ,mech
echRe nocicp or
 Contd
Vestibular Balance Angular MechRec Hair
Accel cells(SCC
Vestibular Balance Linear MechRec Haircells(oto
Accel lith organ)

Olfactory Smell Chem ChemoRec Olf sens

neurn
Gustatory Taste Chem ChemoRec Taste buds
 Properties of Receptors
Specificity: aka Mllers law or doctrine of
specific nerve energies. This refers to the
response given by a particular type of receptor
to a specific sensation. E.g pain receptors give
response to pain sensation etc
Adaptation:decline in discharge of sensory
impulse when a receptor is stimulated
continuously with constant strength. The
rapidly adapting ones are called phasic
receptors(touch and pressure) while the slowly
adapting ones are called tonic
receptors(muscel spindle, pain and cold
receptors)
 Receptors obey Weber-Fechner law:This
law states that the change in response of
a receptor is directly proportional to the
log increase in the intensity of stimulus.
So, to double the response of a receptor,
the strength of stimulus must be
increased 100x
Sensory transduction: A stimulated
receptor is able to convert energy
(stimulus) from the environment into
electrical impulses (action potentials) in
nerve fibres. A process known as
transduction.
 Receptor potential does not obey all or
none law. When the receptor potential is
sufficiently strong (magnitude of about
10mV) action potential is devpd in the
sensory nerve. There is opening of Na+
gated channel leaking to entrance of Na
and devpt of receptor potential and local
circuit of current. This will spread to the
first node of ranvier. Opening of the
voltage gated Na channels in first node of
Ranvier leads to entrance of Na+ and
subsequent generation of action potential
in the nerve fibre.
 Sensory coding: This is the conversion of a
receptor stimulus into a recognizable sensation.
All sensory systems code for four elementary
attributes of a stimulus viz: Modality (type of
energy), Location (site on the body where
stimulus originates), Intensity (response
amplitude or freq of AP), Duration (time from
start to end of a response in a receptor)
Receptor potential: this is a non-propagated
transmembrane potential diff that develops
when a receptor is stimulated. aka generator
potential. It is similar to EPSP in synapse,
endplate potential in NMJ and electrotonic
potential in nerve fibre.
 The Synapse
This is the functional membrane-membrane contact
or junction of a nerve cell with another nerve cell,
an effector cell (muscle or gland) or a sensory
receptor cell. It is the physiological but not
anatomical continuity.
Anatomical Classification: axoaxonic synapse;
Axodendritic synapse, Axosomatic synapse
dendrodendritic
Functional classification:
Electrical synapse: here the physiological continuity
is provided by a gap junction. There is direct
exchange of ions as such the AP reaching the
presynaptic neuron directly enters the postsynaptic
neuron.
Less synaptic delay and impulse travel
in either direction. Seen in cardiac
and smooth muscles of intestine and
epith cells of the lens in eye
Chemical synapse: signals are
transmitted by release of chemical
transmitters. In the chemical
synapse there is no continuity
between the pre and post synaptic
neurons because of the space called
synaptic cleft between the two
neurons. The neurotransmitter
reaching the postsynaptic cause a
 Functions of Synapse
The main function of synapse is impulse
transmission. Some synapses however are
inhibitory. On the basis of this they are
classified as:
Excitatory and Inhibitory
Excitatory Function:
EPSP: A nonpropagated electrical potential
that develops during the process of
synaptic transmission. When AP reaches
the presynaptic terminal voltage gated
Calcium channels are opened to allow entry
of Ca2+ from ECF
 The Ca2+ cause the release of
neurotransmitters from the vesicles by means
of exocytosis. The excitatory neurotransmitter
then reaches the postsynaptic memb via the
cleft and binds with receptor protein forming
a neurotransmitter receptor complex. This
causes opening of ligand gated Na+
channels. Na+ from ECF enter the cell body
of postsynaptic memb leading to mild
depolarization called EPSP which is a local
response in the synapse. If strong enough it
can cause opening of Na+ channels in the
initial segments of the axon with
development of AP
 Inhibitory Function: it can be Presynaptic
inhibition; Postsynaptic inhibition; and
Renshaw inhibition.
Postsynaptic Inhibition: when there is
release of an inhibitory neurotransmitter
e.g GABA, glycine and dopamine from the
presynaptic terminal there is direct
inhibition of impulse transmission. They
can produce IPSP by opening ligand gated
potassium channels as well as chloride
channels. Exit of K+ and influx of Cl- leads
to hyperpolarization which inhibits
transmission
 Presynaptic inhibition:it is the synaptic inhibition
which occurs because of the failure of presynaptic
axon terminal to release the excitatory
neurotransmitter substance. Aka indirect inhibition
Renshaw Cell inhibition: It is the type of synaptic
inhibition which is caused by Renshaw cells in the
spinal cord. These are small motor neurons present
in ant gray horn of spinal cord. When motor
neurons send motor impulses some of the impulse
stimulate the Renshaw cells by passing through
collaterals. In turn the Renshaw cell send inhibitory
impulses to alpha motor neurons so that the
discharge is reduced. The importance of this is that
impulses are adequately selected to omit or block
excesses.
 Poisons like strychnine when
introduced into the body destroys the
inhibitory function at synaptic level
resulting in repeated seizures. In
Parkinsonism the inhibitory system is
impaired resulting in rigidity.