Neuromuscular junction
Overview.
Axon terminal.
Muscle impluse.
End of signal.
Overview.
The brain controls the skeletal muscles, in the body.
Skeletal muscles move the skeleton, which enables the body to move.
Neurons in the motor cortex, in the brain, controls the skeletal muscles.
These neurons send signals to muscles, via the nerves.
These nerves meet the muscles, at the neuromuscular junction.
Neurotransmitters transmit the message from the nerve ending, to the muscle.
This results in a series of actions, in the muscle.
Eventually, the muscle contracts.
Fibres in the muscle structure, are designed to contract and stretch.
Muscle anatomy is discussed in the module Muscle anatomy.
The process of muscle contraction is discussed in the module Muscle contraction.
In this module we will discuss neuromuscular junction.
Axon terminal.
The nerve impulse from the motor neuron,
travels along the axon, to the muscle.
The nerve impulse is an action potential.
The axon terminal is situated at the end of the axon.
The muscle cell is located adjacent to the axon terminal.
The membrane of the muscle cell facing the axon terminal is called the motor end plate.
There is a small gap between the axon terminal, and the motor end plate,
which is called as the synaptic cleft.
Neurotransmitters carry signals from the axon terminal to the motor end plate.
The axon terminal is a semi autonomous unit.
It is a enlarged bulb at the end of the axon terminal.
When the action potential reaches the axon terminal, voltage gated sodium channels open up.
This causes the influx of sodium ions, which results in depolarisation.
The membrane potential starts to increase.
Special calcium channels are present in the axon terminal.
When the membrane potential, reaches a certain threshold value, say plus 10 millivolts,
the calcium channels open up.
This results in a influx of calcium ions.
The axon terminal has a number of vesicles or packets, which stores acetylcholine.
Acetylcholine is the neurotransmitter for activating skeletal muscles.
Acetylcholine is synthesised at the axon terminal.
Acetyl CoA combines with choline, to form acetylcholine.
Calcium ions bind to the acetylcholine vesicles.
This vesicles then fuses with the membrane, in the axon terminal.
The vesicles opens up, and releases its content of acetylcholine, into the synaptic cleft.
This process of releasing substances from a cell, is called exocytosis.
The neurotransmitter diffuses across the synaptic cleft, and reaches the motor end plate.
Muscle impulse.
Muscle cells have a segment, in their membrane,
which interfaces with the axon terminal, of the nerve.
The motor end plate has a number of ligand gated sodium channels.
Acetylcholine binds to these channels.
These channels then open up.
When these channels open up it allows cations like sodium and potassium ions to enter.
The muscle cell is initially at a resting potential, say minus 70 millivolts.
This voltage is closer to the equilibrium potential of potassium, which is minus 85 millivolts.
The equilibrium potential of sodium, is plus 65 millivolts.
The concentration of sodium ions is much higher, outside the membrane,
compared to inside the membrane.
When the channels open up, it causes a large influx of sodium ions into the cell.
Very few potassium ions diffuse out.
For all practical purposes, it acts like a sodium channel.
When one vesicle releases, its contents of acetylcholine,
it causes a small depolarisation, in the motor end plate.
This might be as small as .4 milli volts.
When more acetylcholine is released from the axon terminal,
it causes more sodium channels to open up in the motor end plate.
The net depolarisation, is the summation of all the small depolarisations.
If this reaches a threshold level, it travels along the muscle membrane.
There are voltage gated sodium channels in the muscle membrane.
This depolarisation causes the voltage gated sodium channels to open up.
This causes a way of depolarisation, or action potential,
which propagates across the muscle membrane.
This action potential, acts like a muscle impulse, in muscle cells.
This eventually causes the muscle to contract.
This process is discussed in the module muscle contraction.
We initially started with a nerve impulse, in the axon of the motor nerve.
This electrical signal, is converted into a chemical signal, in the axon terminal.
Acetylcholine carries the chemical signal, across the synaptic cleft, in the neuromuscular junction.
At the motor end plate, the chemical signal, is converted to a electrical signal.
This causes the an action potential in the muscle membrane,
which eventually causes the muscle to contract.
End of signal.
At the end of the signal, from the motor neuron,
no more action potentials, reach the axon terminal.
This effectively stops, any more acetylcholine release.
Some acetylcholine, is already bound to the ligand gated sodium channels.
Some of this diffuse away.
The rest are broken down by a special enzyme.
The release of acetylcholine closes the sodium channel.
No more depolarisation takes place.
This effectively ends the signal, in the muscle membrane.
Eventually the muscle stops the contraction process.
When the brain controls the muscles,
it is not enough to tell the muscles, when to contract.
It is equally important to tell, when to stop contraction.
A simple act, like picking up cup of tea, involves complex signalling,
of different muscles, to start and stop contracting at different times.
The enzyme breaks down acetylcholine, into acetate and choline.
The choline is reabsorbed by the axon terminal.
Mitochondria synthesises acetyl CoA.
The axon terminal synthesises acetylcholine, using the recycled choline.
This ensures that there is a ready and steady supply, of acetylcholine,
in the axon terminal.
The axon terminal is always ready to fire, to signal the muscles.