Neuro-Muscular Junction:
Structure:
Skeletal muscle fibre are innervated by the motor
nerves.
Each nerve divides into many terminal branches.
Each terminal branch supplies one muscle fibre.
The junction between the terminal branch of
nerve fibre and the muscle fibre is called as
Neuro-Muscular Junction(NMJ).
Illustration of the Neuromuscular
Junction
Each terminal branch of the nerve fibre is called
axon terminal.
The terminal portion of axon is expanded like a
bulb and is called as motor end plate.
The end plate invaginates inside the muscle fibre
forming the depression.
This depression is called as synaptic trough or
synaptic gutter.
The motor endplate fits into the synaptic trough.
The membrane of the nerve ending is called as
the pre-synaptic membrane.
The membrane of the muscle fibre is called as
the post-synaptic membrane.
The space between the two is called as the
synaptic cleft.
The axon terminal contains mitochondria and
synaptic vesicles.
The synaptic vesicles contain the
neurotransmitter substance acetylcholine.
The mitochondria contain adenosine
triphosphate(ATP)
ATP is the source of energy for the synthesis of
acetylcholine.
The postsynaptic membrane is thrown into
numerous folds
These folds are called subneural clefts.
The post synaptic membrane contains receptor
proteins called nicotinic acetylcholine
receptors.
NEUROMUSCULAR TRANSMISSION:
The function of neuromuscular junction is to
transmit the impulses from nerve to the muscle.
When the impulses are transmitted from nerve
to muscle, a series of events occur in NMJ.
They are:
1) Release of Acetylcholine
2) Action of Acetylcholine
3) End plate potential
4) Miniature end plate potential
5) Destruction of Acetylcholine
1)Release of acetylcholine:
When the action potential reaches the axon
terminal, it increases the permeability of
presynaptic membrane for calcium ions and the
calcium channels are opened.
The calcium ions enter the axon terminal
from extracellular fluid.
The calcium ions causes the bursting of the
vesicles.
So, the neurotransmitter Ach is released
from the vesicles(Vesicles contains Ach that
is released).
The Ach passes through the presynaptic
membrane and is released into synaptic
cleft.
2)Action of acetylcholine:
The Ach molecules released into the synaptic
cleft bind with the nicotinic receptors present in
the post-synaptic membrane.
The Ach-Receptor complex opens the sodium
channels present in the post-synaptic membrane.
Now, sodium ions from extracellular fluid enter
the NMJ through these channels.
And there, as the sodium ions enters the post-
synaptic membrane, it cause some change in the
electrical potential which is called as the end-
plate potential(EPP).
3) End-plate potential:
The Resting Membrane Potential at NMJ is -
90mV.
When sodium ions enter inside, the end plate
potential occurs.
There is depolarization to -60mV.
4)Miniature End plate potential:
Ach is released in small quantity from the nerve
terminal
Each quantum of Ach produces a weak end
plate potential.
The amplitude of this weak EPP is only upto 0.5
mV and is called as Miniature EPP and it is
unable to cause action potential in the muscle.
When more and more quanta of Ach are
released, the amplitude of potential in endplate
reaches the maximum.
This causes the development of action potential
in the muscle fibre.
5) Fate of Ach:
Within one ms, after the release of ach into
synaptic cleft, it is destroyed by the enzyme
acetylcholine-esterase.
However, Ach is so potent that it can cause the
excitation of muscle fibre within this one ms
itself.
The rapid destruction of Ach prevents the rapid
and repeated excitation of muscle fibre.
Myasthenia Gravis:
Myo- muscle
Asthenia- weakness
Gravis- grave
So myasthenia gravis means muscle weakness.
It is auto-immune disorder where antibodies are
produced against Ach in NMJ. Therefore it is also
known as NMJ disorder.
Due to antibodies against Ach receptors, the
number of ach receptors become less.
Normally, Ach receptors opens the Na channels but
as the Ach receptors reduces, this will decrease the
influx of Na in muscle.
So no action potential is formed in muscle in
response to nerve impulse.
Thus there is in ability to transmit impulse from
nerve to muscle.
Signs and symptoms:
The disease is characterised by rapid onset of
fatigue with marked weakness of all muscles.
The most common muscles are extra-
occular muscles- drooping of eyelids.
Other muscles involved are facial muscles-
loss of facial expression,
masticatory muscles and swallowing
muscles- difficulty in deglutition
In severe case, patient may become bed
ridden and may die due to paralysis of
respiratory muscles.