NEUROMUSCULAR JUNCTION
INTRODUCTION:
Skeletal muscles are innervated by LARGE, MYELINATED nerve fibres.
The junction between the nerve ending and the skeletal muscle fibre is called the Neuromuscular Junction.
STRUCTURE:
1) Axon Terminal/ Motor End Plate:
When the axon comes close to the muscle fibre, it loses its sheath.
So the axis cylinder is exposed. This portion of the axis cylinder is expanded like a bulb and is called as the motor end plate.
It contains Mitochondria and synaptic vesicles (containing neurotransmitter).
Mitochondria contain ATP which is required for the synthesis of Neurotransmittor(acetylcholine).
Thus, Ach is synthesized in the mitochondria and then stored in the synaptic vesicles.
2) Synaptic Trough or Gutter:
Motor end plate invaginates inside the muscle fibre and forms a depression called the synaptic gutter.
3) Synaptic Cleft:
Membrane of the nerve ending is called the Presynaptic Membrane.
Membrane of the muscle fibre is called the Postsynaptic Membrane.(contains receptors for the neurotransmitters)
Space between the presynaptic and postsynaptic membrane is called the synaptic cleft.
4) Subneural Clefts:
The Postsynaptic membrane is thrown into numerous folds called the subneural cleft.
Receptors present on the postsynaptic membrane are called the nicotinic acetylcholine receptors.
NEUROMUSCULAR TRANSMISSION:
It is the transfer of information from the motor nerve ending to the muscle fibre through the neuromuscular junction.
Action potential reaches the axon terminal. There is change in voltage.
This causes the opening of Voltage-gated Calcium channels.
This leads to the INFLUX of calcium ions.
Calcium ions attract the synaptic vesicles towards the presynaptic membrane. Now these vesicles fuse with the presynaptic membrane and thus cause the release of the neurotransmitter(Ach) into the synaptic cleft.
Ach binds with the receptors that are present on the post synaptic membrane.
This causes the opening of the Ligand-GATED Sodium channels.
Influx of Sodium ions from ECF.
This leads to the development of End Plate Potential(EPP).
EPP is a GRADED POTENTIAL. It is non-propagative and causes the development of action potential in the post synaptic terminal which causes excitation-contraction coupling leading to MUSCULAR CONTRACTION.
Destruction of Ach:
The Ach left in the synaptic cleft has to be destroyed rapidly so that re-excitation of the muscle does not occur.
The enzyme Acetylcholinesterase degrades acetylcholine into Inactive Choline and Acetate.
These re-enter the presynaptic terminal, where it is reused in the synaptic vesicle to form NEW ACETYLCHOLINE.
NEUROMUSCULAR BLOCKERS:
Neuromuscular blockers are the drugs that prevent impulse transmission from the nerve fibre to the muscle.
Following are the important neuromuscular blockers, commonly used in clinics and research:
CURARE (receptor blocker):
These combine with acetylcholine receptors and thus prevent the production of EPP.
BUNGAROTOXIN:
It is the toxin derived from the venom of deadly snakes. These also block the Ach receptors.
SUCCINYLCHOLINE AND CARBAMYLCHOLINE:
These act like Ach and keep the muscle in a depolarized state. These are not destroyed by acetylcholinesterase which is why the muscle remains in a depolarized state for a longer period of time.
BOTULINUM TOXIN:
It is derived from the bacteria CLOSTRIDIUM BOTULINUM. It prevents the release of Ach from the presynaptic axon terminal.
DISORDERS OF NMJ:
Myasthenia Gravis:
It is an autoimmune disorder of NMJ caused by antibodies to cholinergic receptors.
Eaton-Lambert Syndrome:
It is an autoimmune disorder caused by antibodies to calcium channels in axon terminal.
FOLLOW ME IN SOCIAL MEDIA
