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the body movements are controlled by muscles.
while contracting, the musle is reduced in length and join closer the 2 bones on which it is inserted.
However , it's the nervous system that controls the muscle cotraction by the means of nerves.
Each nerve cotains thousands of nerve fibers arranged in dendrites which carry out sensory information and axons that convey motor impulses.
Each moter neuron innervates several muscle fibers.
this accociation define what is called a motor unit.
In general , the fewer the muscle fibers are in a motor unit the more the movement is precise.
for example in the temporalis muscle there are 1000 muscle fibers per motor unit.
while in the external ocular muscle there are only 5 ,
this reflect the accuracy of eye movement.
The intensity of the muscle contration is proportional to the number of motor units recruited.
A neuron gives several endings that sometimes scatter throughout the thickness of a muscle,
each terminal is intended to stimulat a single muscle fiber in a specific place the neuromuscular junction.
Just before the axon terminal , the neuron loses its myelin sheath and forms a terminal button.
The terminal button contains many mitochondria that provides energy and several synaptic vesicles.
Each vesicle contains approximately 10,000 of acetylcholine molecules, the unique neurotransmitter of the neuromuscular junction.
On the side of the muscle fiber, we find "The motor end plate", which is the area directly opposit to the terminal button.
The motor end-plate; thick and electrically non-excitable form junctional folds that increase the volume of the synaptic cleft.
Although these two regions are very close to each other there is no real contact between them.
Once it reaches the nerve terminal, the motor impulse causes the opening of calcium channels, triggering an influx of calcium ions inside the cell.
Calcium promotes the fusion of acetylcholine vesicles with the cell membrane releasing their full content of this neurotransmitter in the synaptic cleft.
The acetylcholine molecules diffuse then towards the other side to cholinergic receptors accumulated mainly at the folds.
The binding of two ACh molecules to a receptor causes the opening of a sodium channel that facilitates the entry of sodium ions in the interior of the muscle fiber,
this depolarizes the membrane and creates motor end plate potential.
depending on the number of activated receptors that potential may exceed a threshold and trigger a muscle action potential which will broadcast to the entire muscle membrane and cause a contraction of the muscle fiber.
The acetylcholine molecules are rapidly destroyed by an enzyme "acetyl cholinesterase" present in the synaptic cleft,
this lysis will give 2 molecules of acetate and choline which joins the nerve endings to help form new molecules of acetylcholine.
The rapid destruction of acetylcholine allows to avoid the prolongation of muscle contraction.
There may be a small release of Ach by spontaneous exocytosis in the synaptic cleft without any nerve stimulation, however the number of activated receptors is far from triggering a muscle action potential
The motor unit consist of a motor neuron and all the muscle fibers is innervated
The neurotransmission occurs at the neuromuscular junction that has the terminal buttons, nerve elements and motor endplate which is a muscular element.
When the nerve impulses reach the terminal button, it causes influx of calcium ions inside the cell.
The calcium ion promote the diffusion of synaptic vesicles with the plasma membrane, thereby the release of their contents of acetylcholine.
The acetylcholine molecules bind to bind to their receptors at the endplate, and cause an influx of sodium ions within the cell.
This creates an endplate potential, which trigger muscle action potential and induces a muscle contraction.
The acetylcholine molecules are rapidly degraded by acetylcholinesterase to avoid prolongation of the muscle contraction.
Subtitle by 3BME