DISORDERS OF

SYNAPSES
BY
DR IRAM SADDIQA AAMIR
ASSOCIATE PROFESSOR
BUMDC
KARACHI

LEARNING OBJECTIVES
At the end of lecture, student should be able
to:
DEFINE SYNAPSE.
CLASSIFY SYNAPSE: ANATOMICAL AND
PHYSIOLOGICAL
DESCRIBE PHYSIOLOGICAL ANATOMY OF SYNAPSE.
ENLIST THE DRUGS MODIFYING TRANSMISSION BY
ACTING ON PRESYNAPTIC MEMBRANE, SYNAPSE
AND POST SYNAPTIC MEMBRANE
ENLIST DRUGS THAT ENHANCE OR BLOCK
TRANSMISSION AT THE NEUROMUSCULAR JUNCTION
DESCRIBE THE EFFECTS OF VARIOUS TOXINS ON
SYNPATIC TRANSMISSION

What is a
synapse?
A
junction where
the axon or some
other portion
of
one
cell
(presynaptic
cell)
terminates on the
dendrites, soma, or
axon
of
another
neuron
(post
synaptic cell).
The
term
was
introduced
in
nineteenth century
by
the
British

The Sanger Institute

SYNAPSES
ELECTRICAL SYNAPSES
Open fluid channels that
conduct electricity from
one cell to next.
gap junctions
Two way conduction.
Less time consuming.
eg: Smooth mus: &

cardiac mus:
in the CNS:

Arousal from sleep

Mental attention
Emotions and memory

CHEMICAL SYNAPSES
Almost all synapses of
CNS.
Typically composed of two
parts:
Axonal terminal of the

presynaptic neuron, which

release neurotranmitter.
Receptor region on the
postsynaptic neuron.
NEUROMUSCULAR JUNCTION

Functional Anatomy of a Synapse

The neuromuscular junction is a

synapse
The motor end plate

is the terminal button

of a motor neurone
that makes contact
with a muscle cell
The motor end plate
releases
the
neurotransmitter
acetylcholine
that
ultimately causes the
muscle cell to contract
2008 Paul Billiet

DRUGS THAT ENHANCE OR BLOCK

TRANSMISSION AT NM JUNCTION
1. DRUGS THAT STIMULATE THE MUSCLE

FIBERS LIKE ACETYLCHOLINE LIKE ACTION

Methacholine
Carbachol
Nicotine

2. DRUGS THAT ACT ON SYNAPSE

AND STIMULATE NEUROMUSCULAR
JUNCTION BY INACTIVATING
ACETYLCHOLINESTERASE
NEOSTIGMINE
PHYSOSTIGMINE
DIISOPROPYL FLUOROPHOSPHATE

3. DRUGS THAT BLOCK TRANSMISSION AT NM

JUNCTION
D TUBOCURARINE
CURARE LIKE DRUGS

MYASTHENIA GRAVIS

TOXINS ACTING PRESYNAPTICALLY

BLOCK THE RELAEASE OF NEUROTRANSMITTERS

Synaptobrevin and SNAP-25 are targets of

the clostridial neurotoxins: tetanus toxin acts

in the Central Nervous System (CNS) and
botulinum toxin acts at neuromuscular
synapses paralysis is caused by blockage of
transmitter release.
Neurexin is targeted by a-latrotoxin, the

black widow spider toxin, which induces

massive transmitter release independent of
Ca++ levels.

TETANUS TOXOID
BOTULINUM TOXINS B D F AND G
BOTULINUM TOXIN C

EFFECT OF ALKALOSIS ON SYNAPTIC

TRANSMISSION
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

EFFECT OF ACIDOSIS ON SYNAPTIC

TRANSMISSION
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.

FACTORS
EFFECTINF
TRANSMISSION: DRUGS

SYNAPATIC

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.

THANK YOU