Synapses by Dr Pandian M .

Synapses and Synaptic
Transmission

INTRODUCTION TO SYNAPSE:
•The CNS contains more than 100 billion neurons.
•Incoming signals enter the neuron through synapses
located mostly on the neuronal dendrites, but also on
the cell body.
•For different types of neurons, there may be only a
few hundred or as many as 200,000 such synaptic
connections from input fibers.
•Conversely, the output signal travels by way of a
single axon leaving the neuron.

What is a synapse?
Synapse is the junction between two neurons. It
is not an anatomical continuation.
But, it is only a physiological continuity between two
nerve cells.

What happens at the synapse?
Information is transmitted in the CNS mainly in the form of APs
“=nerve impulse”, which pass from one neuron to another.
Each impulse from its way from one neuron to another may:-
1. Be blocked in its transmission from one neuron to
another
2. Be changed from single impulse to repetitive
impulses.
 Synaptic transmission is a complex process that
permits grading and adjustment of neural activity
necessary for normal function.

CLASSIFICATION OF SYNAPSE
Synapse is classified by two methods:
A. Anatomical classification
B. Functional classification.

Anatomical Types of Synapses
Figure 11.17

Anatomical Types of Synapses
• Axodendritic – synapses between the axon of
one neuron and the dendrite of another
• Axosomatic – synapses between the axon of
one neuron and the soma of another
• Other types of synapses include:
– Axoaxonic (axon to axon)
– Dendrodendritic (dendrite to dendrite)
– Dendrosomatic (dendrites to soma)

Types of synapses ( functional classification
or Types of communication)
A.Chemical synapse
1. Chemical synapses transmission is carried out by
neurotransmitter.
2. Most synapses in human nervous system are of this type.
3. Chemical synapses conduct information only in one
direction.
4. These synapses are more vulnerable to fatigue on repeated
stimulation (synaptic fatigue) and to the effects of hypoxia
and pH changes.
5. Chemical synaptic transmission is definitely slower than
the velocity of nerve conduction resulting in the synaptic
delay.

B. Electrical Synapses
1. Electrical synapses are those in which transmission
occurs through gap junctions
2. It is similar to the process of nerve conduction.
3. The electrical synapses can conduct in both
directions.
4. The speed of transmission at electrical synapses is
the same as that of nerve conduction.
5. Electrical transmission is seen in a few locations in
human nervous system.
6. It is found mainly in invertebrates and lower
vertebrates.

Conjoint synapse refers to a synapse where
both the chemical and electrical transmission
co-exist.
Examples for 2,3  neurons in lateral
vestibular nucleus.

Two principal kinds of synapses: electrical and chemical

Examples of synapses outside CNS
1.NMJ
2.Contact between autonomic neurons and
smooth and cardiac muscles

TYPES OF CHEMICAL SYNAPSES
• On the basis of ultrastructure and
neurotransmitter present the two types of
chemical synapses have been distinguished
• by Golgi: Type I or asymmetric synapses and
type II or symmetric synapses.

SYNAPSE: STRUCTURE & FUNCTIONS
Synaptic cleft: This the space between the
axon terminal and sarcolemma. It has a width of
200-300 angstroms

Action of the transmitter substance on
post-synaptic neuron:
At the synapse, the membrane of post-synaptic
neuron contains large number of receptor
proteins.

These receptors have two components
1. Binding site that face the
cleft to bind the
neurotransmitter
2. Ionophore: It passes all the way through the
membrane to the interior. It is of two types
Ion channels 2nd messenger system in
the post-synaptic
membrane.
This mechanism is
important where
prolonged post-synaptic
changes are needed to
stay for days, months.
Years (memory).
Channels are not suitable
for causing prolonged
post-synaptic changes as
they close in milliseconds.
Cation channels
Na+ (most common)
K+,Ca++,
Opening of Na+
channels  
membrane potential in
positive direction
toward threshold level
of excitation  (+)
neuron
Anion channels
Cl¯ (mainly)
Opening of Cl¯
channels  diffusion
of negative charges
into the membrane
  membrane
potential making it
more negative 
away from threshold
level  (-) neuron

1. Opening of ion channel [open for prolonged time]
2. Activation of cAMP  long-term changes [memory]
3. Activation of intracellular enzymes  cellular
chemical activators
4. Activate gene transcription  protein + structural
changes [memory] long-term memory
Most common type of 2nd messenger
in neurons is G-protein
The second messenger system

Chemical synapses: the predominant means of communication
between neurons

Electrical events in post-synaptic neurons:
1. RMP of neuronal soma:
~ 65mV i.e. less than sk. ms. [70 to 90mV]
- If the voltage is less negative  the neuron is
excitable
Causes of RMP:
1.Leakage of K+ (high K+ permeability)
2.Large number of negative ions inside: proteins,
phosphate
3.Excess pumping of Na+ out by Na+-K+ pump

2. Effect of synaptic excitation on post-synaptic
membrane:
= Excitatory post-synaptic potential [EPSPs]
When excitatory neurotransmitter bind to its receptor
on post-synaptic membrane 
partial depolarization [ Na influx] of post-synaptic
cell membrane immediately under presynaptic
ending, i.e. EPSPs
If this potential rises enough to threshold level  AP
will develop and excite the neuron (central or
neuronal summation)

This summation will cause the membrane potential
to increase from 65mV to 45mV.
 EPSPs = +20mV which reaches the membrane to
the firing level  AP develops at axon hillock.
N.B. Discharge of single pre-synaptic terminal can
never increase the neuronal potential from 65mV to
45mV.
EPSP is produced by the action of an excitatory
neurotransmitter  depolarization of post-synaptic
membrane.

The excitatory neurotransmitter opens Na+ or Ca + +
channels  depolarization of the area under the
pre-synaptic membrane.
EPSPs:
• Graded response
• Proportionate to the strength of the stimulus
• Can be summated
• If large enough to reach firing level  AP is
produced
Post-synaptic potential of +10 to +20mV is needed
to produce AP
Excitatory Postsynaptic Potential

Inhibitory post-synaptic potentials
Stim. of some inputs [=pre-synaptic terminals] 
hyperpolarization of the post-synaptic memb. which is the
IPSP.
Causes: it is produced by localized increase in membrane
permeability to Cl¯ of post-synaptic memb. (produced by
inhibitory neurotransmitter)   excitability and memb.
potential becomes away from firing level.
Also IPSP can be produced by:-
-Opening of K+ channels  outward movement of K+
-Closure of Na+ or Ca++ channels
-IPSP = 5mV

Fate of neurotransmitter
After a transmitter substance is released at a synapse,
it must be removed by:-
Diffusion out of synaptic cleft into
surrounding fluid
Enzymatic destruction e.g. Ach esterase for
Ach
Active transport back into pre-synaptic
terminal itself e.g. norepinephrine
Neurotransmitter bound to a postsynaptic neuron:
1. Produces a continuous postsynaptic effect
2. Blocks reception of additional “messages”

Synaptic properties
1. One-way conduction
Synapses generally permit conduction of
impulses in one-way i.e. from pre-synaptic
to post-synaptic neuron.

2. Synaptic delay
Is the minimum time required for transmission
across the synapse.
This time is taken by
Discharge of transmitter substance by pre-synaptic
terminal
Diffusion of transmitter to post-synaptic
membrane
Action of transmitter on its receptor
Action of transmitter to  membrane permeability
Increased diffusion of Na+ to  post-synaptic
potential

Properties of synapses (con…)
3. Synaptic inhibition
Types:
A. Direct inhibition
B. Indirect inhibition
C. Reciprocal inhibition
D. Inhibitory interneuron
E. Feed forward inhibition
F. Lateral inhibition

A. Direct inhibition
Post-synaptic inhibition, e.g. some interneurones in
sp. cord that inhibit antagonist muscles.
Neurotransmitter secreted is Glycine.
Occurs when an inhibitory neuron (releasing
inhibitory substance) act on a post-synaptic neuron
leading to  its hyperpolarization due to opening
of Cl¯ [IPSPs] and/or K+ channels.

B. Indirect inhibition
Pre-synaptic inhibition.
This happens when an inhibitory synaptic knob
lie directly on the termination of a pre-synaptic
excitatory fiber.
The inhibitory synaptic knob release a
transmitter which inhibits the release of
excitatory transmitter from the pre-synaptic
fiber.
The transmitter released at the inhibitory knob
is GABA.
The inhibition is produced by  Cl¯ and  K+.
e.g. occurs in dorsal horm  pain gating.

C. Reciprocal inhibition
•Inhibition of antagonist activity is initiated in
the spindle in the agonist muscle.
• Impulses pass directly to the motor neurons
supplying the same muscle and
•via branches to inhibitory interneurones that
end on motor neurones of antagonist muscle.

D. Inhibitory interneuron
( Renshaw cells)
Negative feedback inhibitory interneuron of a
spinal motor neuron .
This feedback inhibition also occurs in:
Cerebral cortex
Limbic system
Note that Renshaw cells are
in spinal cord

E. Feed forward inhibition
occurs in the cerebellum to limit the duration of
excitation.
F. Lateral inhibition
Because of lateral inhibition, the lateral
pathways are inhibited more strongly. This
happens in pathways utilizing most accurate
localization. e.g. movement of skin hairs
can be well located, temperature and pain
are poorly located.

4. Summation
a)Spatial summation.
When EPSP is in more than one synaptic
knob at same time.
a)Temporal summation.
If EPSP in pre-synaptic knob are
successively repeated without significant
delay so the effect of the previous
stimulus is summated to the next

5. Convergence and divergence
Convergence
When many pre-synaptic neurones
converge on any single post-synaptic
neuron.
Divergence
Axons of most pre-synaptic neurons divide
into many branches that diverge to end on
many post-synaptic neuron.

6.Occlusion
 Expected response due to pre-synaptic
fibers sharing post-synaptic neurone
[=overlap].
Neuromodulation: non-synaptic action of
a substance on neurons that alters their
sensitivity to synaptic stimulation or
inhibition. e.g. neuropeptides, steroids

7. Fatigue
Exhaustion of nerve transmitter. Fatigue:
If the pre synaptic neurons are continuously
stimulated there may be an exhaustion of the
neurotransmitter. Resulting is stoppage of
synaptic transmission.
The post synaptic membrane become less
sensitive to the neurotransmitter.

8. Long-term potentiation = LTP
Rapidly developing persistent
enhancement of post-synaptic potential
response to pre-synaptic stim. after brief
period of rapidly repeated stimulation of
pre-synaptic neurone.
Ca++ intracellular in post-synaptic
membrane.
 Amygdala N-methyl-D-aspartate NMDA
receptors.

9. Long-term depression
First noted in Hippocampus
Later shown Through brain
Opposite of LTP
 synaptic strength
Caused by slower of pre-synaptic neurone
Smaller rise of Ca++
Occure in amino 3 hydroxy -5-
methylisoxazole4-propionate AMPA recep

FACTORS EFFECTINF SYNAPATIC
TRANSMISSION: ALKALOSIS
• Normally, alkalosis greatly increases neuronal
excitability.
• For instance, a 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.
•The overbreathing blows off carbon dioxide and
therefore elevates the pH of the blood momentarily

TRANSMISSION: ACIDOSIS
Conversely, acidosis greatly depresses neuronal
activity;
A fall in pH from 7.4 to below 7.0 usually
causes a comatose state.
For instance, in very severe diabetic or uremic
acidosis, coma virtually always develops.

TRANSMISSION: DRUGS
•Many drugs are known to increase the excitability
of neurons, and others are known to decrease
excitability.
• For instance, Caffeine, Theophyline,
Theobromine, which are found in coffee, tea, and
cocoa, respectively,
• All increase neuronal excitability, presumably by
reducing the threshold for excitation of neurons.

TRANSMISSION: DRUGS
•Strychnine is one of the best known of all agents that
increase excitability of neurons.
•However, it does not do this by reducing the threshold for
excitation of the neurons; instead, it inhibits the action of
some normally inhibitory transmitter substances,
•especially the inhibitory effect of glycine in the spinal
cord.
•Therefore, the effects of the excitatory transmitters
become overwhelming,
•and the neurons become so excited that they go into
rapidly repetitive discharge, resulting in severe tonic
muscle spasms.

REFRENCES
 1.Text book of medical physiology
-Guyton and hall, 12th edition.
 2.Ganong’s review of medical physiology
-23rd edition
 3.text of medical physiology
-2nd edition
 4.net sources (acknowledge for all online sources)
 5.text book of medical physiology
--A.K. JAIN
 6.text book of medical physiology
---indu khurana


Synapses by Dr Pandian M .

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