This document provides information about synapses and synaptic transmission in the central nervous system (CNS). It defines a synapse as the junction between two neurons and discusses the key anatomical structures involved, including the presynaptic terminal, synaptic cleft, and postsynaptic membrane. It describes how an action potential in the presynaptic neuron leads to calcium ion influx and neurotransmitter release into the synaptic cleft. The neurotransmitters then bind to receptors on the postsynaptic membrane, which can result in excitation via EPSPs or inhibition via IPSPs depending on the specific neurotransmitter and receptor type involved. Higher-level functions such as learning and memory emerge from the complex integration of signals at numerous synapses throughout the CNS neural circuits.

1. - Dr. Chintan
Synapse

2. Sensory System

3. Motor System

4. CNS Synapses
 information is transmitted in the CNS mainly in the
form of nerve action potentials, called simply “nerve
impulses,” through a succession of neurons, one after
another.
 However, in addition, each impulse
 (1) may be blocked in its transmission from one neuron
to the next,
 (2) may be changed from a single impulse into
repetitive impulses, or
 (3) may be integrated with impulses from other
neurons to cause highly complicated patterns of
impulses in successive neurons.

5. Definition
The junction between two
neurons is called synapse.
This word was first
introduced by
SHERRINGTON .

6. Characteristic
 It is not an Anatomical continuity but just a
Physiological contiguity (contact without
connection).
 Thus a synapse is a functional junction
between two neurons.
 It is the most important determinant of CNS
function as information is passed from one
neuron to other via a synapse.

7. Functions of
synapse
 1) Transmission of impulses to and
fro from periphery to CNS and vice
versa.
 2) Modification of impulses,
integration of impulses or changing
or blocking of impulses .
 3) Higher function of CNS like
learning, memory etc are possible

8. Types of synapses
1) Anatomical classification -
depending upon the part of neurons
involved.
2) Physiological classification -
depending upon the nature of
transmission through the synapse.
3) According to number of neurons
involved.

9. Types of Synapses — Chemical and
Electrical
 Almost all the synapses used for signal
transmission in the CNS of the human being are
chemical synapses.
 In these, the first neuron secretes at its nerve
ending synapse a chemical substance called a
neurotransmitter
 and this transmitter in turn acts on receptor
proteins in the membrane of the next neuron to
excite the neuron, inhibit it, or modify its sensitivity
in some other way.

10. Types of Synapses — Chemical and
Electrical
 Electrical synapses are characterized by direct
open fluid channels that conduct electricity from
one cell to the next.
 Most of these consist of small protein tubular
structures called gap junctions that allow free
movement of ions from the interior of one cell to the
interior of the next.
 Only a few gap junctions have been found in CNS
 it is by way of gap junctions and other similar
junctions that action potentials are transmitted from

11. “One-Way” Conduction
 Chemical synapses always transmit the signals
in one direction:
 that is, from the neuron that secretes the
transmitter substance, called the presynaptic
neuron, to the neuron on which the transmitter
acts, called the postsynaptic neuron.
 This is the principle of one-way conduction at
chemical synapses, and it is quite different from
conduction through electrical synapses, which
often transmit signals in either direction.

12. Anatomical
classification
 1) Axodendritic synapse - Type I (most common)
- motor neurons of spinal cord, excitatory synapse
in cerebral cortex, climbing fibers of cerebellum.
 2) Axosomatic synapse - Type-II (less common) -
motor neurons of spinal cord, basket cells of
cerebellum, autonomic ganglia.
 3) Axoaxonic synapse (least common) - seen in
spinal cord.
 4) Dendrodendritic synapse (rare) - seen in
olfactory bulb between mitral and granule cell.

14. Physiological or functional
classification
1) Chemical Synapse
2) Electrical Synapse
3) Conjoint Synapse (where
both chemical and electrical
transmission coexists)

15. Differences between chemical and
electrical synapse
 Chemical synapse
 1) Transmission is by
Neurotransmitters.
 2) Most of the synapses are
of this type.
 3) They conduct in one
direction.
 4) More vulnerable to fatigue
on repeated stimulation,
hypoxia, PH changes.
 5) Slow speed causing
synaptic delay as it allows for
large no of synapses per
neuron.
 Electrical synapse
 1) Transmission is by gap
junctions – low resistance
bridges - ions pass easily
 2) Seen in some places eg
retina, olfactory bulb,
hippocampus, cerebral
cortex.
 3) They conduct in both
directions.
 4) Insensitive to hypoxia.
 5) Rapid efficient
transmission with no delay
as not too many synapses
per neuron.

16. Physiologic Anatomy of the Synapse

17. Structure of a synapse
Pre synaptic terminal
Pre synaptic membrane
Synaptic cleft
Postsynaptic terminal or
process

19. Presynaptic terminals
 Electron Microscope studies show that
there are various anatomical forms
hence called by different names,
terminal knobs, buttons, end feet or
synaptic knobs.
 There is no myelin sheath and each
knob has Mitochondria and synaptic
vesicles containing neurotransmitter
substance.

20. Pre synaptic terminals on
dendrites & soma
1) Some of these presynaptic
terminals are excitatory — that is,
they secrete a transmitter
substance that excites the
postsynaptic neuron.
2) But other presynaptic terminals
are inhibitory — they secrete a
transmitter substance that inhibits

21. Synaptic vesicles- different
types
 1) Round or spherical clear vesicles
 Have excitatory NTs eg, Ach, Glutamate
 2) Flat clear vesicles
 Have inhibitory NTs eg, GABA, Glycine
 3) Small dense core vesicles
 Have catecholamines - E/NE, Dopamine
 4) Large dense core vesicles
 Peptide NTs – Endorphin, Enkephalin

22. Axoplasmic transport of
vesicles
The vesicles and the proteins
contained in their walls are
synthesized in the Golgi apparatus
in the neuronal cell body and
 migrate down the axon to the
endings by fast Axoplasmic
transport.

23. Presynaptic membrane
 It is the axonal membrane of the
synaptic terminal.
 It contains large no. of calcium gated
channels (Active zone - a thickened
area)
 These voltage gated Ca channels open
when an Action Potential depolarizes
the presynaptic membrane.

24. Synaptic cleft
 It is a small gap of 200-300 angstrom
width (20-40 nm) between pre and
postsynaptic membranes.
 It is filled with ECF containing some
glycoproteins.
 The NTs is released in this cleft.

25. Post synaptic terminal or
process
It is the name of the receiving
neuron eg dendritic spine, or
soma,
where synaptic knob
synapses.

26. Post synaptic
membrane
It is the membrane lining the
postsynaptic process.
It contains a large no of receptor
proteins which protrude into the
synaptic cleft.
NTs released in the cleft bind to
receptor proteins to cause the

27. Mech - AP causes release of NTs
from presynaptic terminal - Ca role
 The presynaptic membrane contains large
numbers of voltage-gated calcium channels.
 When an action potential depolarizes the
presynaptic membrane, these calcium
channels open and allow large numbers of
calcium ions to flow into the terminal.
 The quantity of transmitter substance that
is then released from the terminal into the
synaptic cleft is directly related to the
number of calcium ions that enter.

28.  When the calcium ions enter the presynaptic
terminal - they bind with special protein
molecules on the inside surface of the
presynaptic membrane, called release sites.
 This binding in turn causes the release sites
to open through the membrane,
 allowing a few transmitter vesicles to
release their transmitter into the cleft after
each single action potential.

29. Clinical application
 Clinically, tetanus toxin causes spastic paralysis
by blocking presynaptic transmitter release in the
CNS and
 botulism causes flaccid paralysis by blocking the
release of acetylcholine at the neuromuscular
junction.
 On the positive side, however, local injection of
small doses of botulinum toxin has proved
effective in the treatment of a wide variety of
conditions characterized by muscle hyperactivity.
 Examples include injection into the lower
esophageal sphincter to relieve achalasia and

30. Receptors on postsynaptic
membrane
 They have two important components-
 (1) a binding component that
protrudes outward from the membrane
into the synaptic cleft— here it binds the
neurotransmitter coming from the
presynaptic terminal and
 (2) ionophore component that passes
all the way through the postsynaptic

31. Ionophore component is of two
types
 (1) an ion channel that allows passage of
specified types of ions through the membrane
or
 (2) a “second messenger” activator is a
molecule that protrudes into the cell
cytoplasm and activates one or more
substances inside the postsynaptic
neuron.
 These substances in turn serve as “second

32. Ion channels- two types
 (1) cation channels that most often
allow sodium ions to pass when
opened, but sometimes allow
potassium and/or calcium ions as
well, and
 (2) anion channels that allow mainly
chloride ions to pass but also minute
quantities of other anions.

33. Cation channel opens - excitation
anion channel opens - inhibition
 when cation channels open and allow
positively charged sodium ions to enter, the
positive electrical charges of the sodium
ions will in turn excite this neuron.
 Therefore, a transmitter substance that opens
cation channels is called an excitatory
transmitter.
 Conversely, opening anion channels allows
negative electrical charges to enter, which
inhibits the neuron.
 Therefore, transmitter substances that open
these channels are called inhibitory

34. Rapid opening or closing of ion
channels
 When a transmitter substance
activates an ion channel, the channel
usually opens within a fraction of a
millisecond;
 when the transmitter substance is no
longer present, the channel closes
equally rapidly.
 The opening and closing of ion
channels provide a means for very

35. Second messenger system - via G
protein causes 4 effects
 1) opening an ion channel (K channel) in
the membrane of the second neuron;
 2) activating an enzyme system in the
neuron’s membrane Eg – ATP-cAMP or
GTP – cGMP
 3) activating an intracellular enzyme
system;
 4) causing gene transcription in the

36. Post – Synaptic events

37. Excitatory or Inhibitory Receptors
 Excitation
 1. Opening of sodium channels to allow large numbers
of positive electrical charges to flow to the interior of the
postsynaptic cell.
 This raises the intracellular membrane potential in the
positive direction up toward the threshold level for
excitation.
 2. Depressed conduction through chloride or
potassium channels
 This decreases the diffusion of negatively charged
chloride ions to the inside of the postsynaptic neuron or
decreases the diffusion of positively charged
potassium ions to the outside.

38. Excitatory or Inhibitory Receptors
 Excitation
 3. Various changes in the internal metabolism of the
postsynaptic neuron to excite cell activity or,
 to increase the number of excitatory membrane
receptors or decrease the number of inhibitory
membrane receptors
 Inhibition
 1. Opening of chloride ion channels through the
postsynaptic neuronal membrane.
 This allows rapid diffusion of negatively charged
chloride ions from outside the postsynaptic neuron to the
inside,

39. Excitatory or Inhibitory Receptors
 Inhibition
 2. Increase in conductance of potassium ions out
of the neuron.
 This allows positive ions to diffuse to the
exterior, which causes increased negativity inside
the neuron; this is inhibitory.
 3. Activation of receptor enzymes that inhibit
cellular metabolic functions
 increase the number of inhibitory synaptic
receptors or decrease the number of excitatory

40. Synaptic transmission
 Arrival of A P in axon terminal (synaptic knob)
 --- Depolarization of presynaptic terminal
 --- Opening of voltage gated Ca channels in
presynaptic memb
 --- Influx of Ca from ECF of synaptic cleft into
presynaptic terminal
 --- exocytosis of vesicles & release of NTs into
synaptic cleft
 --- Binds to receptors on post synaptic membrane
to form a complex

41. Electrical Events

42. Excitatory NT- Na entry – EPSP
- AP
 if excitatory then opening of Na channels with
influx of Na from ECF into postsynaptic
 ---Development of EPSP
 ---With more & more opening of Na channels
in initial segment of axon
 ---When excitation reaches critical level
 --- Action Potential develops which spreads
through the axon of postsynaptic neuron.
 Glutamate is one such excitatory NT.

43. Inhibitory NT - Cl, K -
IPSP
 If it is an inhibitory synapse then NT
 --- Receptor complex causes opening of
K or Cl channels
 --- causing Hyperpolarisation
 --- IPSP
 --- inhibition thus occurs.
 GABA, Glycine are inhibitory NTs

44. EPSP - Excitatory post synaptic
potential
 It is depolarization of post synaptic memb,
produced by excitatory NT eg Glutamate.
 Ionic basis of EPSP– excitatory NT binds to
receptor protein to open up ligand gated Na
channels of postsynaptic memb.
 Thus rapid entry of Na ions change RMP of -65mv
to -45mv called EPSP.
 Discharge of single presynaptic terminal does
not cause potential change of -65 to -45mv so
simultaneous discharge of many (40-80) leads
to this thus causing Summation

45. Excitatory Postsynaptic Potential -
EPSP

46. Properties of EPSP
 1) It is similar to receptor potential &
end plate potential.
 2) It is non propagative hence differs
from AP.
 3) It does not obey All or None law
 5) It shows temporal and spatial

47. IPSP - Inhibitory post synaptic
potential
 both chloride influx and potassium efflux
increase the degree of intracellular negativity,
which is called hyperpolarization.
 This inhibits the neuron because the
membrane potential is even more negative
than the normal intracellular potential.
 Therefore, an increase in negativity beyond
the normal resting membrane potential level
is called an inhibitory postsynaptic potential
(IPSP).

48. Inhibitory Postsynaptic Potential -
IPSP

49. Synaptic Transmitters
 One group - small-molecule, rapidly acting
transmitters - most acute responses of the nervous
system,
 transmission of sensory signals to the brain
 motor signals back to the muscles.
 The other group is made up of a large number of
neuropeptides of much larger molecular size that
are slowly acting - More prolonged actions
 long-term changes in numbers of neuronal
receptors,
 long-term opening or closure of certain ion

52. Initial Segment of the Axon
 When the EPSP rises high enough in the
positive direction, there comes a point at which
this initiates an action potential in the neuron.
 the action potential begins in the initial segment
of the axon where the axon leaves the neuronal
soma.
 The main reason for this point of origin of the
action potential is that the soma has relatively
few voltage-gated sodium channels in its
membrane,
 which makes it difficult for the EPSP to open

53. Initial Segment of the Axon
 the membrane of the initial segment has
seven times as great a concentration of
voltage-gated sodium channels as does
the soma and,
 therefore, can generate an action potential
with much greater ease than can the soma.
 The EPSP that will elicit an action potential in
the axon initial segment is between +10 and
+20 millivolts.
 This is in contrast to the +30 or +40 millivolts

54. Excitation and spread of
AP

55. Types of synaptic
inhibition
1. Pre synaptic
inhibition
2. Renshaw Cell
inhibition

56. Presynaptic Inhibition
 In addition to inhibition caused by inhibitory synapses
operating at the neuronal membrane - postsynaptic
inhibition,
 another type of inhibition often occurs at the presynaptic
terminals before the signal ever reaches the synapse -
presynaptic inhibition
 Presynaptic inhibition is caused by release of an
inhibitory substance onto the outsides of the
presynaptic nerve fibrils before their own endings
terminate on the postsynaptic neuron – GABA
 This has a specific effect of opening anion channels,
allowing large numbers of chloride ions to diffuse into
the terminal fibril.
 The negative charges of these ions inhibit synaptic

57. Importance of pre synaptic
inhibition
 Presynaptic inhibition occurs in
many of the sensory pathways in the
nervous system. Seen in pain
pathways – gating of pain transmission -
so pain control occurs.
 adjacent sensory nerve fibers often
mutually inhibit one another, which
minimizes sideways spread and mixing
of signals in sensory tracts

59. Renshaw cell inhibition
 Here neurons inhibit themselves in a negative
feedback manner.
 It is seen in spinal cord which has motor neurons like
alpha motor neurons situated in anterior gray horn.
 Renshaw cell is a type of motor neuron near alpha
motor neuron.
 When alpha sends impulses via ant nerve root fibres
- some of its impulses reach the Renshaw cells by
collaterals, which excites them.
 Renshaw cell in turn sends inhibitory impulses to
alpha motor neurons and thus inhibits them.

61. Post synaptic inhibition
 It is also called direct inhibition.
 It is due to the development of IPSP.
 It is due to failure of production of AP in post
synaptic membrane because of release of
inhibitory NT from pre synaptic terminal.
 Sometimes it may occur also due to refractory
period – postsynaptic membrane can be
refractory to excitation because it has just fired
and is in refractory state.

62. Feed forward inhibition
 Seen in the cerebellum in basket cells and
Purkinje cells.
 When impulse passes through afferent
nerve both the cells are stimulated but
basket cells in turn inhibit Purkinje cells.
 So duration of discharge by Purkinje cells
is reduced and output from it is controlled.

63. Significance of synaptic
inhibition
 1) It offers restriction over neurons and
muscles so that excess stimuli are
inhibited and various movements are
performed properly and accurately.
 2) Inhibition helps to select exact no of
impulses and to block the excess ones.
 3) Poison like strychnine destroys all
inhibitory functions causing convulsions
- post synaptic inhibition.
 4) In disorders like Parkinsonism

64. Fate of NT
 The NT is inactivated as follows,
 1) By diffusion out of the cleft
 2) Enzymatic degradation of NT, eg
dissociation of Ach by acetylcholinesterase
enzyme.
 3) Reuptake of NT back into presynaptic
membrane.

65. Importance of inhibition
Persistence of NT in synaptic
cleft produces prolong
stimulation of post synaptic
neuron
in response to a single
electrical impulse in pre

66. synapse
1) One way conduction (Law of
forward conduction).
2) Synaptic delay.
3) Synaptic fatigue.
4) Convergence and
Divergence.
5) Summation.
6) Occlusion phenomenon.

67. synapse
8) Facilitation.
9) Reverberation.
10) Reciprocal inhibition.
11) After discharge.
12) Effect of acidosis and hypoxia.
13) Effect of drugs.
14) Synaptic plasticity and

68. One Way Conduction
 The chemical synapse allows only one way
conduction i.e. from presynaptic to
postsynaptic neuron and never in opposite
direction.
 This is also called Bell-Magendie Law.
 It occurs because NT is present only at
presynaptic area and postsynaptic has
specific receptor sites.
 Hence antidromically conducted signal dies
out at soma due to lack of chemical substance.
 Significance- for orderly neural function.

69. Synaptic Delay
 During transmission of a neuronal signal from a
presynaptic neuron to a postsynaptic neuron, a
certain amount of time is consumed in the process of
 (1) discharge of the transmitter substance by the
presynaptic terminal,
 (2) diffusion of the transmitter to the postsynaptic
neuronal membrane,
 (3) action of the transmitter on the membrane receptor,
 (4) action of the receptor to increase the membrane
permeability,
 (5) inward diffusion of sodium to raise the excitatory
postsynaptic potential to a high enough level to elicit an

70. Significance of delay
 1) Conduction along a chain of neurons
is slow if there are many synapses.
 2) It is possible to know if reflex
pathway is monosynaptic or
polysynaptic by measuring the delay
in transmission of impulse from dorsal to
ventral root across the spinal cord.

71. Summation
 It is of two types,
 1)Spatial Summation— When many
presynaptic terminals are stimulated
simultaneously there is summation or
fusion of effects in postsynaptic neuron.
 2)Temporal Summation— When one
presynaptic terminal is stimulated
repeatedly.
 Summation causes progressive
increase in EPSP which causes

72. Spatial Summation

74. Temporal Summation
 Each time a presynaptic terminal fires, the released
transmitter substance opens the membrane channels
for at most a millisecond
 But the changed postsynaptic potential lasts up to 15
milliseconds after the synaptic membrane channels have
already closed.
 Therefore, a second opening of the same channels can
increase the postsynaptic potential to a still greater level,
 and the more rapid the rate of stimulation, the greater
the postsynaptic potential becomes.
 Thus, successive discharges from a single
presynaptic terminal, if they occur rapidly enough, can
add to one another; that is, they can “summate.” -
temporal summation.

76. Occlusion
phenomenon
 It means that when there is simultaneous
stimulation of two presynaptic neurons
 the response is less than the sum total of the
response obtained when they are stimulated
separately.
 For eg presynaptic neuron A & B upon stimulation
separately each stimulates 10 post synaptic
neurons making total of 20,
 But when A & B are stimulated simultaneously they
stimulate less eg 15 postsynaptic neurons only.
 This decrease in response is due to some post
synaptic neurons being common to both
presynaptic neurons.

77. Occlusion
 the response to stimulation of B
and C together is not as great
as the sum of responses to
stimulation of B and C
separately,
 because B and C both end on
neuron Y.
 This decrease in expected
response, due to presynaptic
fibers sharing postsynaptic
neurons, is called occlusion

78. Occlusion (2+2=3)

79. Subliminal fringe 2+2 = 5
 Opposite to occlusion
 Response obtained by the simultaneous
stimulation of two presynaptic neurons is
greater than the sum total of the response
obtained when they are separately stimulated
 Suppose stimulation of neuron A causes
stimulation of 5 post synaptic neurons and
stimulation of neuron B causes stimulation
of 5 postsynaptic neurons and then sum of
neurons stimulated is 10
 But when neuron A and B are stimulated
simultaneously number of the postsynaptic

80. Subliminal fringe 2+2 = 5
 Subliminal means below threshold
 Fringe means border.
 Thus the post synaptic neurons are said to be
in a subliminal fringe if they are not discharged
by activity of pre synaptic neurons but their
excitability is increased.
 Those which have discharged are in
discharging zone and have fired due to
development of AP in them whereas
 those in periphery (fringe) are excited up to
sub threshold level only and AP is not

81. Neuronal pool – supra, sub, thresold

83. Synaptic plasticity
Plasticity refers to the capability of
being easily moulded or changed.
Synaptic transmission can easily be
increased or decreased on the basis of
past experience.
These changes can be presynaptic or
postsynaptic in location and play an

84. Forms of synaptic plasticity
1) Post tetanic Potentiation
2) Long term Potentiation
3) Long term Depression
4) Habituation
5) Sensitization

85. Post tetanic Potentiation
Tetanizing stimuli in pre synaptic
neuron results in increase
postsynaptic potentials lasting for
minutes to hours.
Cause is increase Ca influx in pre
synaptic neuron which increases
release of NTs.

86. Long term Potentiation
If post tetanic potentiation gets
more prolonged and lasts for days
it is called as long term potentiation.
Cause is due to increase
intracellular Ca in post synaptic
neuron rather than presynaptic.
This occurs in HIPPOCAMPUS

87. Long term depression
It is opposite of long term
potentiation.
There is slower stimulation of
presynaptic neurons, with
decrease in synaptic conduction
following decreased Ca influx.
Seen commonly in Hippocampus

88. Habituation
 When a stimulus is benign and is repeated
over and over, the response to the
stimulus gradually disappears
(habituation).
 This is associated with decreased release of
neurotransmitter from the presynaptic
terminal because of decreased
intracellular Ca2+.
 The decrease in intracellular Ca2+ is due to
a gradual inactivation of Ca2+ channels.
 It can be short-term, or it can be prolonged if

89. Sensitization
There is prolong occurrence of
increased postsynaptic responses
after a stimulus is paired once
or several times with a noxious
stimulus.
It is due to Ca mediated changes
- adenyl cyclase that results in
greater production of cAMP.

90. Facilitation
When presynaptic neuron is
stimulated with several successive
individual stimuli,
each stimulus may evoke a larger
post synaptic potential than that
evoked by the previous stimulus.

91. “Facilitation” of Neurons
 Often the summated postsynaptic potential is
excitatory but has not risen high enough to
reach the threshold for firing of the postsynaptic
neuron.
 When this happens, the neuron is said to be
facilitated – its membrane potential is nearer
the threshold for firing than normal, but not yet at
the firing level.
 Consequently, another excitatory signal
entering the neuron from some other source
can then excite the neuron very easily.
 Diffuse signals in the nervous system often

92. Fatigue of Synaptic Transmission
 When excitatory synapses are repetitively stimulated
at a rapid rate,
 the number of discharges by the postsynaptic neuron is at
first very great, but the firing rate becomes progressively
less in succeeding milliseconds or seconds - fatigue of
synaptic transmission.
 Fatigue is an exceedingly important characteristic of
synaptic function because when areas of the nervous
system become overexcited, fatigue causes them to
lose this excess excitability after awhile.
 Fatigue is probably the most important means by which
the excess excitability of the brain during an epileptic
seizure is finally unresponsive so that the seizure stops.
 Thus, the development of fatigue is a protective

93. Fatigue of Synaptic Transmission
 The mechanism of fatigue is mainly exhaustion or partial
exhaustion of the stores of transmitter substance in
the presynaptic terminals.
 The excitatory terminals on many neurons can store
enough excitatory transmitter to cause only about
10,000 action potentials,
 and the transmitter can be exhausted in only a few
seconds to a few minutes of rapid stimulation.
 Part of the fatigue process probably results from two other
factors as well:
 (1) progressive inactivation of many of the postsynaptic
membrane receptors and
 (2) slow development of abnormal concentrations of ions
inside the postsynaptic neuronal cell.

94. Effect of Acidosis or Alkalosis
 Alkalosis greatly increases neuronal excitability - rise in
arterial blood pH from the 7.4 norm to 7.8 to 8.0 often
causes cerebral epileptic seizures because of
increased excitability of some or all of the cerebral
neurons.
 This can be demonstrated especially well by asking a
person who is predisposed to epileptic seizures to
overbreathe
 overbreathing blows off carbon dioxide and therefore
elevates the pH of the blood momentarily, but even
this short time can often precipitate an epileptic attack.
 acidosis greatly depresses neuronal activity - a fall in

95. Effect of Hypoxia
 Neuronal excitability is also highly
dependent on an adequate supply of
oxygen.
 Cessation of oxygen for only a few
seconds can cause complete
inexcitability of some neurons.
 This is observed when the brain’s blood
flow is temporarily interrupted, because

96. Effect of Drugs
 caffeine, theophylline, and theobromine, which
are found in coffee, tea, and cocoa, respectively,
all increase neuronal excitability, presumably by
reducing the threshold for excitation of neurons.
 Most anesthetics increase the neuronal membrane
threshold for excitation and thereby decrease
synaptic transmission at many points in the nervous
system.
 Because many of the anaesthetics are especially
lipid soluble - change the physical

97. Divergence of Signals
 An amplifying type of divergence - an input signal spreads to
an increasing number of neurons as it passes through
successive orders of neurons in its path.
 corticospinal pathway in its control of skeletal muscles, with
a single large pyramidal cell in the motor cortex capable of
exciting as many as 10,000 muscle fibers.
 divergence into multiple tracts - the signal is transmitted in two
directions
 information transmitted up the dorsal columns of the spinal
cord takes two courses in the lower part of the brain:
 (1) into the cerebellum and
 (2) on through the lower regions of the brain to the thalamus
and cerebral cortex.
 in the thalamus, almost all sensory information is relayed
both into still deeper structures of the thalamus and at the

99. Convergence of Signals
 Convergence means signals from multiple inputs
uniting to excite a single neuron.
 convergence from a single source - multiple
terminals from a single incoming fiber tract
terminate on the same neuron.
 The importance of this is that neurons are never
excited by an action potential from a single input
terminal.
 But action potentials converging on the
neuron from multiple terminals provide enough
spatial summation to bring the neuron to the

100. Convergence of Signals
 Convergence can also result from input signals (excitatory or
inhibitory) from multiple sources
 the interneurons of the spinal cord receive converging signals
from
 (1) peripheral nerve fibers entering the cord,
 (2) propriospinal fibers passing from one segment of the cord to
another,
 (3) corticospinal fibers from the cerebral cortex, and
 (4) several other long pathways descending from the brain into the
spinal cord.
 Then the signals from the interneurons converge on the anterior
motor neurons to control muscle function.
 Such convergence allows summation of information from different
sources, and the resulting response is a summated effect of all
the different types of information.

102. Neuronal Circuit with Both Excitatory and Inhibitory
Signals
 Sometimes an incoming signal to a neuronal pool
causes an output excitatory signal going in one direction
and at the same time an inhibitory signal going
elsewhere.
 at the same time that an excitatory signal is
transmitted by one set of neurons in the spinal cord to
cause forward movement of a leg,
 an inhibitory signal is transmitted through a separate
set of neurons to inhibit the muscles on the back of the
leg so that they will not oppose the forward movement.
 This type of circuit is characteristic for controlling all

104. Afterdischarge
 a signal entering a pool causes a prolonged output discharge,
called afterdischarge, lasting a few milliseconds to as long as
many minutes after the incoming signal is over.
 Synaptic Afterdischarge. When excitatory synapses
discharge on the surfaces of dendrites or soma of a
neuron,
 a postsynaptic electrical potential develops in the neuron and
lasts for many milliseconds, especially when some of the long-
acting synaptic transmitter substances are involved.
 As long as this potential lasts, it can continue to excite the
neuron, causing it to transmit a continuous train of output
impulses
 Thus, as a result of this synaptic “afterdischarge” mechanism
alone, it is possible for a single instantaneous input signal to

105. Reverberatory (Oscillatory) Circuit
 Such circuits are caused by positive feedback
within the neuronal circuit that feeds back to re-
excite the input of the same circuit.
 So, once stimulated, the circuit may discharge
repetitively for a long time.
 Involvement of only a single neuron.
 the output neuron simply sends a collateral nerve
fiber back to its own dendrites or soma to
restimulate itself.
 once the neuron discharges, the feedback
stimuli can keep the neuron discharging for a

107. Reverberatory (Oscillatory) Circuit
 a few additional neurons in the feedback circuit, which
causes a longer delay between initial discharge and the
feedback signal
 both facilitatory and inhibitory fibers impose on the
reverberating circuit.
 A facilitatory signal enhances the intensity and
frequency of reverberation, whereas an inhibitory signal
depresses or stops the reverberation.
 most reverberating pathways are constituted of many
parallel fibers - At each cell station, the terminal fibrils
spread widely.
 The total reverberating signal can be either weak or

110. Receptor Potentials
 Whatever the type of stimulus that excites the receptor, its
immediate effect is to change the membrane electrical
potential of the receptor. This change in potential is called a
receptor potential.
 Different receptors can be excited in one of several ways to
cause receptor potentials:
 (1) by mechanical deformation of the receptor, which
stretches the receptor membrane and opens ion channels;
 (2) by application of a chemical to the membrane, which also
opens ion channels;
 (3) by change of the temperature of the membrane, which
alters the permeability of the membrane; or
 (4) by the effects of electromagnetic radiation, such as light
on a retinal visual receptor, which either directly or indirectly
changes the receptor membrane characteristics and allows

113. Adaptation of Receptors
 characteristic of all sensory receptors is that they
adapt either partially or completely to any constant
stimulus after a period of time.
 when a continuous sensory stimulus is applied, the
receptor responds at a high impulse rate at first
and then at a progressively slower rate until finally
the rate of action potentials decreases to very few or
often to none at all.
 complete adaptation of a mechanoreceptor is about
2 days, which is the adaptation time for many carotid
and aortic baroreceptors.
 the non mechanoreceptors — the chemoreceptors

114. Slowly Adapting Receptors - tonic
receptors
 Slowly adapting receptors continue to transmit
impulses to the brain as long as the stimulus is
present - they keep the brain constantly informed of
the status of the body and its relation to its
surroundings.
 impulses from the muscle spindles and Golgi
tendon apparatuses allow the nervous system to
know the status of muscle contraction and load on
the muscle tendon
 (1) receptors of the macula in the vestibular
apparatus,

115. Rapidly Adapting Receptors
 Rate Receptors, Movement Receptors, Phasic Receptors
 Receptors that adapt rapidly cannot be used to transmit a
continuous signal because these receptors are stimulated only
when the stimulus strength changes - they react strongly while a
change is actually taking place.
 sudden pressure applied to the tissue excites pacinian
corpuscle for a few milliseconds, and then its excitation is
over even though the pressure continues.
 But later, it transmits a signal again when the pressure is
released.
 the pacinian corpuscle is important in informing the nervous
system of rapid tissue deformations, but it is useless for

116. Thank You…