THE NERVOUS SYSTEM:

GENERAL PRINCIPLES AND SENSORY

PHYSIOLOGY

Organization of the Nervous System, Basic

Functions of Synapses, and Neurotransmitters
NEURON - THE BASIC FUNCTIONAL
UNIT
 The central nervous system
contains more than 100
billion neurons.
 signals enter in the neuron
through synapses.
 Conversely, the output signal
travels by way of a single
axon leaving the neuron.
 this axon has many separate
branches to other parts of the
nervous system or peripheral
body.
 A special feature of
most synapses is that
the signal normally
passes only in the
forward direction,
from the axon of a
preceding neuron to
dendrites on cell
membranes of
subsequent neurons.
SENSORY PART OF THE NERVOUS SYSTEM - SENSORY RECEPTORS

 Most activities of the nervous system are

initiated by sensory experiences that excite
sensory receptors,
 These sensory experiences can either cause
immediate reactions from the brain, or
memories of the experiences can be stored in
the brain for minutes, weeks, or years and
determine bodily reactions in the future.
 SENSORY PART OF THE NERVOUS SYSTEM - SENSORY RECEPTORS

 somatic portion of the sensory

system transmits sensory
information from the receptors of
the body surface and from deep
structures.
 This information enters the central
nervous system through peripheral
nerves and is conducted to
multiple sensory areas in (1) the
spinal cord at all levels; (2) the
reticular substance of the medulla,
pons, and mesencephalon of the
brain; (3) the cerebellum; (4) the
thalamus; and (5) areas of the
cerebral cortex.
MOTOR PART OF THE NERVOUS SYSTEM-EFFECTORS
 The most importal role of the nervous system is to control the
various bodily activities.
 This is achieved by controlling

 (1) contraction of skeletal muscles,

 (2) contraction of smooth muscle in the organs,

 and (3) secretion of active

chemical substances by both

exocrine and endocrine glands.
 These activities are collectively called motor functions of the

nervous system,
 and the muscles and glands are called effectors because they are

the actual anatomical structures that perform the functions

dictated by the nerve signals.
 MOTOR PART OF THE NERVOUS SYSTEM-EFFECTORS
 This picture shows the "skeletal" motor nerve part
of the nervous system for controlling skeletal
muscle contraction.
 Although we have another part of nervous system,
called the autonomic nervous system, for
controlling smooth muscles, glands, and other
internal bodily systems;
 the skeletal muscles can be controlled from many
levels of the central nervous system: (1) the
spinal cord; (2) the reticular substance of the
medulla, pons, and mesencephalon; (3) the basal
ganglia; (4) the cerebellum; and (5) the motor
cortex.
 the lower regions concerned primarily with
automatic, instantaneous muscle responses to
sensory stimuli, and the higher regions with
difficult complex muscle movements controlled
by the thought processes of the brain.
 "INTEGRATIVE" FUNCTION OF THE NERVOUS SYSTEM

 One of the most important functions of the nervous system is to process

incoming information in such a way that appropriate mental and motor
responses will occur.
 But, when important sensory information excites the mind, it is immediately

channeled into integrative and motor regions of the brain to cause

responses.
 This channeling and processing of information is called the integrative

function of the nervous system.

Thus, if a person places a hand on a hot stove, the desired instantaneous
response is to lift the hand.
And other associated responses follow, such
as moving the entire body away from the
stove and perhaps even shouting with pain.
ROLE OF SYNAPSES IN PROCESSING INFORMATION
 The synapse is the junction between 2 neurons.
 synapses determine the directions of spreading of nervous signals.
 Some synapses transmit signals from one neuron to the next with ease, others

transmit signals with difficulty.

 facilitatory and inhibitory signals

from other areas in the nervous

system can control synaptic
transmission, sometimes opening
the synapses for transmission or
closing them.
 some postsynaptic neurons

respond with large numbers of output

impulses, and others respond with only
a few.
 STORAGE OF INFORMATION-MEMORY
 Only a small fraction of even the most
important sensory information usually causes
immediate motor response.
 But much of the information is stored for
future control of motor activities and for use in
the thinking processes.
 Most storage occurs in the cerebral cortex, but
even the basal regions of the brain and the
spinal cord can store small amounts of
information.
 The storage of information is the process we
call memory, and this, too, is a function of the
synapses.
 Each time certain types of sensory signals pass
through sequences of synapses, these synapses
become more capable of transmitting the same
type of signal the next time, a process called
facilitation.
MAJOR LEVELS OF CENTRAL NERVOUS SYSTEM FUNCTION

 3 major levels of the  :(1) the spinal cord

central nervous system
are
level,
 (2) the lower brain
or subcortical level,
 and (3) the higher
brain or cortical
level.
SPINAL CORD LEVEL
 Even after the spinal cord has been cut in the high neck region,
many highly organized spinal cord functions still occur.
 neuronal circuits in the cord can cause (1) walking movements,

(2) reflexes that withdraw portions of the

body from painful objects, (3) reflexes that
control local blood vessels, gastrointestinal
movements, or urinary excretion.
 In fact, the upper levels of the nervous

system often operate not by sending

signals directly to the periphery of the
body but by sending signals to the control
centers of the cord, simply "commanding"
the cord centers to perform their functions.
 LOWER BRAIN OR SUBCORTICAL LEVEL
 Many activities of the body are controlled
by lower brain - in the medulla, pons,
mesencephalon, hypothalamus,
thalamus, cerebellum, and basal
ganglia.
 For instance, subconscious control of
arterial pressure and respiration is
achieved in the medulla and pons.
 Control of equilibrium is a function of the
older portions of the cerebellum and the
reticular substance of the medulla, pons,
and mesencephalon.
 many emotions, such as anger, excitement,
sexual response, reaction to pain, can still
occur after destruction of much of the
cerebral cortex.
 HIGHER BRAIN OR CORTICAL LEVEL

 the cerebral cortex is an extremely large memory

storehouse.
 The cortex never functions alone but always in

association with lower centers of the nervous

system.
 Without the cerebral cortex,

the functions of the lower brain

centers are often imprecise.
the cerebral cortex is essential
For most of our thought.
Each portion of the nervous system performs
specific functions.
But it is the cortex that opens a world of stored
information for use
by the mind.
CENTRAL NERVOUS SYSTEM SYNAPSES

 Information is transmitted in the central nervous

system mainly in the form of nerve action
potentials, called simply "nerve impulses,"
through a succession of neurons, one after
another.
 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,

(3) may be integrated with impulses from other

neurons.
"ONE-WAY" CONDUCTION AT CHEMICAL SYNAPSES

 Chemical synapses have important characteristic!

 They always transmit the signals in one direction:
 from the neuron that secretes the transmitter substance, (presynaptic
neuron), to the neuron on which the transmitter acts(the postsynaptic
neuron).
 This is the principle of one-way conduction at chemical synapses,
 it is quite different from conduction through electrical synapses, which
often transmit signals in either direction.
 the one-way conduction mechanism allows signals to be directed toward
specific goals.
 STRUCTURE OF NEURON (MOTORNEURON)
 It is composed of 3 major parts:
 the soma, which is the main body of the neuron;
 single axon, which extends from the soma into a peripheral;
 the dendrites, which are great numbers of branching projections
of the soma.
 STRUCTURE OF SYNAPSE
 many synaptic knobs called presynaptic terminals lie on the
surfaces of the dendrites and soma of the motor neuron.
 These presynaptic terminals are the ends of nerve fibers that
originate from many other neurons.
 Many of these presynaptic terminals are excitatory- they secrete a
transmitter substance that excites the postsynaptic neuron.
 But other presynaptic terminals are inhibitory-they secrete a
transmitter substance that inhibits the postsynaptic neuron.
Neurons in other parts of the cord and brain differ from the
anterior motor neuron in
 (1) the size of the cell body;
 (2) the length, size, and number of dendrites,;

 (3) the length and size of the axon;

 (4) the number of presynaptic terminals.
 PRESYNAPTIC TERMINALS
 the presynaptic terminals are sometimes called terminal knobs, boutons,
end-feet, or synaptic knobs.
 The presynaptic terminal is separated from the postsynaptic neuronal soma

by a synaptic cleft.
 The terminal has 2 internal important structures of the synapse: the

transmitter vesicles and the mitochondria.

 The transmitter vesicles contain the transmitter substance that, when

released into the synaptic cleft, either

excites or inhibits the
postsynaptic neuron-excites
if the neuronal membrane
contains excitatory receptors,
inhibits if the membrane
contains inhibitory receptors.
 The mitochondria provide

adenosine triphosphate
(ATP).
 When a action potential
spreads over a presynaptic
terminal,
 Depolatization of its
membrane causes vesicles
to empty into the cleft.
 The released transmitter
causes an immediate
change in permeability of
the postsynaptic membrane,
 This leads to excitation or
inhibition of postsynaptic
neuron.
MECHANISM BY WHICH AN ACTION POTENTIAL CAUSES TRANSMITTER RELEASE
FROM THE PRESYNAPTIC TERMINALS

 The membrane of the

presynaptic terminal is
called the presynaptic
membrane.
 It contains large numbers of
voltage-gated Ca2+
channels.
 When an action potential
spreads and depolarizes the
presynaptic membrane,
Ca2+channels open and
Ca2+ flow into the terminal.
.
 The quantity of transmitter
substance that is released into the
synaptic cleft is directly related
to the number of Ca2+ that enter.
 When the Ca2+ enter the
presynaptic terminal, it is
believed that they bind with
special protein molecules on the
inside surface of the presynaptic
membrane, called release sites.
 This binding causes the release
sites to open through the
membrane, allowing a few
transmitter vesicles to release
their transmitter into the cleft.
ACTION OF THE TRANSMITTER SUBSTANCE ON THE POSTSYNAPTIC NEURON
 The receptors of the
postsynaptic membrane
have 2 important
components:
 (1) a binding component –
outside of the mrmbrane -
here it binds the
neurotransmitter,
 (2) an ionophore
component - that passes all
the way through the
postsynaptic membrane to
the interior of the
postsynaptic neuron.
 The ionophore is one of 2
types:
 (1) an ion channel - allows
passage of ions through the
membrane or
 (2) a "second messenger"
activator - it is a molecule that
protrudes into the cell
cytoplasm and activates
substances inside the
postsynaptic neuron. These
substances serve as "second
messengers" to increase or
decrease specific cellular
functions.
 ION CHANNELS

The ion channels in the postsynaptic

neuronal membrane are usually of 2
types:

1) cation channels that (2) anion channels that

most often allow Na+ to allow mainly Cl- to pass,
pass, but sometimes also minute quantities of
allow K+ and/or Ca2+ other anions.
 The cation channels that
conduct Na+ are lined ION CHANNELS
with negative charges.
 These charges attract
Na+ into the channel
when the channel
diameter increases to a
size larger than that of
the hydrated Na+.
 But those same negative
charges repel Cl- and
other anions and prevent
their passage.
 ION CHANNELS

 For the anion channels, when the channel diameters

become large enough, Cl- pass into the channels
and on through to the opposite side,
 whereas Na+, K+, Ca2+are blocked, mainly because
their hydrated ions are too large to pass.
 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 transmitters.
"SECOND MESSENGER" SYSTEM IN THE POSTSYNAPTIC NEURON

 Many functions of the nervous system (memory)

-require prolonged changes in neurons after the
initial transmitter substance is gone.
 The ion channels are not suitable for causing
prolonged postsynaptic neuronal changes because
these channels close within milliseconds after the
transmitter substance is no longer present.
 prolonged postsynaptic neuronal excitation or
inhibition is achieved by activating a "second
messenger" chemical system.
 One of the most common types
of second messenger systems
uses a group of proteins called
G-proteins.
 G-protein is attached to the
receptor.
 The G-protein consists of
3components:
 (α) component - the activator
portion of the G-protein
 (β) and (γ) components are
attached to the alpha component
and to the inside of the cell
membrane.
 On activation by a nerve impulse, the alpha portion of the
G-protein separates from the beta and gamma portions.
 Inside the cytoplasm, the alpha component performs
different functions, depending on the specific characteristic
of neuron.
1.
1. Opening
Opening ion
ion channels
channels through
through the
the
postsynaptic
postsynaptic cell
cell membrane.
membrane.
this
this channel
channel (K+)
(K+) stays
stays open
open for
for aa
prolonged
prolonged time,
time, in
in contrast
contrast to
to rapid
rapid
closure
closure of
of directly
directly activated
activated ion
ion channels.
channels.
2.
2. Activation
Activation of of cyclic
cyclic adenosine
adenosine
monophosphate
monophosphate (cAMP) (cAMP) or or cyclic
cyclic
guanosine
guanosine monophosphate
monophosphate (cGMP)(cGMP) in in
the
the neuronal
neuronal cell.
cell.
cAMP
cAMP or or cc GMP
GMP activate
activate specific
specific
metabolic
metabolic reactions
reactions inin the
the neuron
neuron and
and
initiate
initiate long-term
long-term changes
changes in
in cells.
cells.
3. Activation of intracellular enzymes.
The G-protein can directly activate one or more
intracellular enzymes.
the enzymes can cause many specific chemical
functions in the cell.
4. Activation of gene transcription.
This is one of the most important effects of
activation of the second messenger systems
because gene transcription can cause formation of
new proteins within the neuron.
Some postsynaptic receptors,
when activated, cause
excitation of the postsynaptic
neuron, and others cause
inhibition.
 EXCITATION
 1. Opening of Na+ to
allow positive electrical
charges to flow to the
interior of the
postsynaptic cell.
 This raises the membrane
potential in the positive
direction up toward the
threshold level for
excitation.
 EXCITATION
2. decrease of conduction through CL- or K+
channels, or both.
This decreases the diffusion of Cl- to the inside of
the postsynaptic neuron or diffusion of K+ to the
outside.
In either instance, the effect is to make the
internal membrane potential more positive
than normal, which is excitatory.
 EXCITATION
 3. Various changes in the internal metabolism of
the postsynaptic neuron to excite cell activity or,
in some instances, to increase the number of
excitatory membrane receptors or decrease the
number of inhibitory membrane receptors.
This allows rapid diffusion
Opening of Cl-
Cl- from outside the
channels through
postsynaptic neuron to the
the postsynaptic
inside,
neuronal
carrying negative
chargesmembrane.
inward.
INHIBITION
 INHIBITION

2. Increase in conductance of K+
out of the neuron.

This allows positive ions

to diffuse to the exterior,
which causes increased
negativity inside the
neuron;
 INHIBITION

3. Activation of receptor enzymes that inhibit cellular

metabolic functions that increase the number of
inhibitory synaptic receptors or decrease the number
of excitatory receptors.
 CHEMICAL SUBSTANCES THAT FUNCTION AS SYNAPTIC TRANSMITTERS

We have 2 groups of synaptic transmitters.

One group consists of small-molecule, rapidly acting transmitters.

The other consists of a large number of neuropeptides of much larger molecular size that
are usually much more slowly acting.
SMALL MOLECULE, RAPIDLY ACTING TRANSMITTERS

CLASS 1 CLASS 2 – the CLASS 3-amino acids CLASS 4

amines

  Acetylcholine   Norepinephrine   Gamma-aminobutyric Nitric oxide (NO)

acid (GABA)

  Epinephrine   Glycine

  Dopamine   Glutamate

  Serotonin   Aspartate

  Histamine
 NEUROPEPTIDE, SLOWLY ACTING TRANSMITTERS OR GROWTH FACTORS
Hypothalamic-releasing h. Pituitary peptides Peptides that act on gut From other tissues
and brain

Thyrotropin-releasing Adrenocorticotropic Leucine enkephalin Angiotensin2

hormone hormone (ACTH)

Luteinizing hormone- β-endorphin Methionine enkephalin Bradykinin

releasing h

Somatostatin (growth α-melANOCYTE- Vasoactive intestinal cARNOSINE

h.inhibitory factor) STIMULATING h. polypeptide (vip)

Prolactin Gastrin Sleeo peptides

Luteinizing hormone Cholecystokinin Calcitonin

Thyrotropin Nerve growth factor

Growth hormone Brain derived neurotropic
factor

Vasopressin Substance P
Oxytocin Neurotensin
Insulin
Glucagon
 The small-molecule,
rapidly acting transmitters - they cause acute The neuropeptides cause prolonged actions
responses of the nervous system

- long-term changes in numbers of receptors,

- long-term opening or closure of ion
transmission of sensory signals to the brain
channels,
or motor signals back to the muscles.
- long-term changes in numbers of synapses
- or sizes of synapses.
 ACETYLCHOLINE
 Its synthesis is in the presynaptic terminal from acetyl coenzyme
A and choline in the presence of the choline acetyltransferase.
 Then it is transported into its specific vesicles.
 When the vesicles release the acetylcholine , the acetylcholine is
rapidly split again to acetate
 And choline by the enzyme

cholinesterase.
 then, inside the presynaptic

terminal, the vesicles are

recycled; choline is actively
transported back into the
terminal for synthesis of new
acetylcholine
ACETYLCHOLINE IS SECRETED BY NEURONS IN MANY AREAS OF THE NERVOUS SYSTEM

(1) the terminals of the large pyramidal cells from the

motor cortex,

(2) several different types of neurons in the basal

ganglia,

(3) the motor neurons that innervate the skeletal muscles,

ACETYLCHOLINE IS SECRETED BY NEURONS IN MANY AREAS OF THE NERVOUS SYSTEM BUT SPECIFICALLY BY

(4) the preganglionic neurons of the autonomic nervous

system,

(5) the postganglionic neurons of the parasympathetic

nervous system

(6) some of the postganglionic neurons of the

sympathetic nervous system.
ACETYLCHOLINE
●
In most instances, acetylcholine
has an excitatory effect;

however, it has inhibitory effects at some

●

peripheral parasympathetic nerve endings,

●
such as inhibition of the heart
by the vagus nerves.
 NOREPINEPHRINE

is secreted by the many neurons

whose cell bodies are located in the
brain stem and hypothalamus.

Is secreted by neurons in the locus ceruleus in the pons.

activates excitatory receptors, but in a few areas, it

activates inhibitory receptors.

it is also secreted by most postganglionic neurons of the

sympathetic nervous system
THE MORE IMPORTANT SMALL-MOLECULE TRANSMITTERS

Dopamine is secreted by neurons in the

substantia nigra.
The effect of dopamine is usually inhibition.

Glycine is secreted mainly in the

spinal cord. an inhibitory transmitter.

GABA (gamma-aminobutyric acid) is secreted

in the spinal cord, cerebellum, basal ganglia,
and many areas of the cortex. cause inhibition.
THE MORE IMPORTANT SMALL-MOLECULE TRANSMITTERS

Glutamate is secreted in many of the

sensory pathways . It causes
excitation.
Serotonin is secreted by nuclei raphe of the brain stem
and project to many brain and spinal cord areas. acts as an
inhibitor of pain pathways in the cord, and an inhibitor
action in the higher regions of the nervous system
Nitric oxide is secreted in areas of the brain responsible for long-
term behavior and memory. It is different from other small-
molecule transmitters in its mechanism of formation in the
presynaptic terminal and in its actions. It is not preformed and
stored in vesicles. it is synthesized almost instantly as needed,
 NEUROPEPTIDES

 The neuropeptides are not synthesized in the

presynaptic terminals.
 they are synthesized by ribosomes in the neurons
body.
 the neuropeptides are generally a thousand or
more times as potent as the small-molecule
transmitters.
 they often cause much more prolonged actions -
prolonged closure of Ca2+ channels, prolonged
changes in the metabolism of cells, and/or
prolonged alterations in numbers of excitatory or
inhibitory receptors.
EXCITATORY POSTSYNAPTIC POTENTIAL

 this is the resting neuron with an unexcited

presynaptic terminal resting on its surface. The
resting membrane potential everywhere in the
soma is -65 millivolts.
EXCITATORY POSTSYNAPTIC POTENTIAL

 This is a presynaptic terminal that has secreted an

excitatory transmitter into the cleft.
 The transmitter acts on the excitatory receptor to
increase the membrane's permeability to Na+.
 Na+ diffuse rapidly to the inside of the membrane.
EFFECT OF SYNAPTIC EXCITATION ON THE POSTSYNAPTIC MEMBRANE-EXCITATORY
POSTSYNAPTIC POTENTIAL

 As a result of the rapid influx of Na+ to the interior, the

resting membrane potential has increased in the positive
direction from -65 to -45 millivolts.
 This positive increase in voltage is called the excitatory
postsynaptic potential (or EPSP)
 In this case, the EPSP is +20 millivolts-, 20 mv more
positive than the resting value.
GENERATION OF ACTION POTENTIALS IN THE INITIAL SEGMENT OF THE AXON LEAVING THE NEURON

 When the EPSP rises high enough in the positive

direction, there comes a point at which this
initiates an action potential in the neuron.
GENERATION OF ACTION POTENTIALS IN THE INITIAL SEGMENT OF THE AXON LEAVING THE NEURON

 the action potential does not begin adjacent to the

excitatory synapses.
 it begins in the initial segment of the axon
where the axon leaves the neuronal soma.
 The main reason - is that the soma has few voltage-gated Na+
channels, which makes it difficult for the EPSP to open the required
number of Na+ channels to elicit an action potential.
 Conversely, the membrane of the initial segment has 7 times as great
a concentration of voltage-gated Na+ 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.
 Once the action potential begins, it travels peripherally
along the axon and
 usually also backward over the soma.
 In some instances it travels backward into the dendrites
but not into all of them
 because they, like the neuronal soma, have very few
voltage-gated Na+ channels and frequently cannot
generate action potentials at all.
EFFECT OF INHIBITORY SYNAPSES ON THE POSTSYNAPTIC MEMBRANE-INHIBITORY
POSTSYNAPTIC POTENTIAL

 The inhibitory synapses open mainly Cl- channels.

 negatively charged CL- ions move from the extracellular fluid to
the interior, which will make the interior membrane potential
more negative than normal, approaching the -70 millivolt.
 Opening K+ channels allow positively charged potassium ions to
move to the exterior, the interior membrane potential become
more negative than usual.
EFFECT OF INHIBITORY SYNAPSES ON THE POSTSYNAPTIC MEMBRANE-INHIBITORY
POSTSYNAPTIC POTENTIAL

 both Cl- influx and K+ efflux increase 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).
 PRESYNAPTIC INHIBITION

 We have another type of inhibition that often occurs at the

presynaptic terminals .
 This type of inhibition is called presynaptic inhibition.
 Presynaptic inhibition is caused by release of an inhibitory
substance outside of the presynaptic neuron (axon).
 In most instances, the inhibitory transmitter substance is GABA
(gamma-aminobutyric acid).
 PRESYNAPTIC INHIBITION

 GAMA causes opening anion channels, allowing large numbers of

Cl- to diffuse into the axon.
 The negative Cl- inhibit synaptic transmission because they cancel
much of the excitatory effect of the positive Na+ that also enter
the axon when an action potential arrives.
 Presynaptic inhibition occurs in many of the sensory pathways in
the nervous system.
 "SPATIAL SUMMATION" IN NEURONS
 Excitation of a single
presynaptic axon never
excites the neuron.
 The reason for this is that
the amount of transmitter
substance released by a
single terminal to cause an
EPSP is usually no greater
than 0.5 to 1 millivolt,
instead of the 10 to 20
millivolts normally required
to reach threshold for
excitation.
 many presynaptic terminals
are usually stimulated at the
same time.
 "SPATIAL SUMMATION" IN NEURONS
 Even though these terminals are
spread over wide areas of the
neuron, their EPSP can still
summate;
 they can add to one another until
excitation does occur.
 When the EPSP becomes great
enough, the threshold for firing
will be reached and an action
potential will develop
spontaneously in the initial
segment of the axon.
 This effect of summing
simultaneous EPSP by activating
multiple terminals on widely
spaced areas of the neuron is
called spatial summation.
 "TEMPORAL SUMMATION"

 Each time a presynaptic terminal fires, the

released transmitter substance opens the
membrane channels for at most a millisecond.
 But the postsynaptic potential lasts up to 15
milliseconds after the synaptic membrane
channels have already closed.
 so, 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.
 "TEMPORAL SUMMATION"

 Thus, successive discharges from a single presynaptic

terminal, if they occur rapidly enough, can add to one
another;
 they can "summate." This type of summation is called
temporal summation.
 SIMULTANEOUS SUMMATION OF INHIBITORY AND EXCITATORY POSTSYNAPTIC
POTENTIALS
 if a neuron is being excited by an EPSP, an inhibitory
signal from another source can often reduce the
postsynaptic potential to less than threshold value for
excitation, thus block the activity of the neuron
"FACILITATION" OF NEURONS

 Often the summated postsynaptic potential is

excitatory but has not risen high enough to reach the
threshold for firing by the postsynaptic neuron.
 When this happens, the neuron is said to be
facilitated.
 That is, 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.
"EXCITATORY STATE" OF NEURON
FATIGUE OF SYNAPTIC TRANSMISSION
 When excitatory synapses are repetitively
stimulated rapidly, the number of discharges by
the postsynaptic neuron is at first very great, but
then the firing rate becomes progressively less.
 This is called fatigue of synaptic transmission.
 when parts of the nervous system become
overexcited, fatigue causes losing this excess
excitability after a while.
 The mechanism of fatigue is mainly exhaustion
of the stores of transmitter substance in the
presynaptic terminals.
 FATIGUE OF SYNAPTIC TRANSMISSION

fatigue is probably the most important means by

which the excess excitability of the brain during an
epileptic seizure finally decreases.
Thus, the development of fatigue is a protective
mechanism against excess neuronal activity.
EFFECT OF ACIDOSIS OR ALKALOSIS ON SYNAPTIC TRANSMISSION
 Most neurons are highly responsive to changes in
pH of the surrounding interstitial fluids.
 alkalosis greatly increases neuronal excitability.
 a rise in arterial blood pH from the 7.4 to 7.8 to
8.0 often causes cerebral epileptic seizures
because of increased excitability of some cerebral
neurons.
EFFECT OF ACIDOSIS OR ALKALOSIS ON SYNAPTIC TRANSMISSION

acidosis greatly decreases neuronal activity;

a fall in pH from 7.4 to below 7.0 usually causes a comatose state.

For instance, in diabetic acidosis, coma always develops.

ACIDOSIS – is an icreased acidity in
the blood and other body tissue, ALKALOSIS is a condition reducing H+
concentration of arterial blood.

Is an increased H+ concentration,

alkalosis is said to occur when pH of the

blood exceeds 7.45.

Acidosis is said to occur when arterial

pH fall below 7,35.
 EFFECT OF HYPOXIA ON SYNAPTIC TRANSMISSION

 Neuronal excitability is
highly dependent on an
supply of O2.
 Lack of O2 for only a few
seconds can cause
inexcitability of some
neurons.
 when the brain's blood
flow is temporarily
interrupted within 3 to 7
seconds, the person
becomes unconscious.
 EFFECT OF DRUGS ON SYNAPTIC TRANSMISSION

 Many drugs increase the excitability of neurons,

and others decrease excitability.
 For instance, caffeine, theophylline, and
theobromine, which are found in coffee, tea, and
cocoa,
 increase neuronal excitability, by reducing the
threshold for excitation of neurons.
EFFECT OF DRUGS ON SYNAPTIC TRANSMISSION
 Strychnine can increase excitability of neurons.
 it inhibits the action of some inhibitory transmitters,
especially glycine in the spinal cord.
 the neurons become so excited that they go into rapidly
repetitive discharge, resulting in severe tonic muscle
spasms.
EFFECT OF DRUGS ON SYNAPTIC TRANSMISSION

Most anesthetics increase the neuronal membrane threshold for excitation and
so decrease synaptic transmission.

Because many of the anesthetics are lipid soluble, they change the structure of the
neuronal membranes, making them less responsive to excitatory agents.