Motor Plate: Definition, Parts, Synapses and Diseases That Affect The Neuromuscular Union

It is called the neuromuscular junction that occurs between the motor neuron and the muscle fiber.

This neuromuscular junction plays an elementary role in transmitting nerve signals or impulses from the motor neuron to the muscle fiber that causes muscle contraction.

Thus, we can say that the neuromuscular junction is associated with the motor neuron or nerve cell and muscle fiber.

This part of the muscle fiber attached interacts with the motor neuron is a synapse between the “end synaptic bulbs” present in the motor neuron and the “endplate of the engine” located in the muscle fiber.

The motor endplate is a highly excitable region in the plasma membrane of the muscle fiber and is responsible for initiating potential action movements through the muscle surface.

This effect finally results in muscle contraction.

Parts of the neuromuscular junction

The neuromuscular junction is composed of:


The presynaptic neuron or the presynaptic bulb:

Each nerve cell has a cell body and branches. These branches that transfer a signal to the nerve cell are called numerous dendrites.

The branch that is responsible for carrying the message or signal to the outside of the nerve cell or neuron is called the axon.

The axon is one, and it is the zone of the motor neuron that ends in the area of contact of the muscle, in a structure of the oval form of about 32 microns of extension.

This bulbous inflammation is also called the presynaptic end bulb.

At this distal end of the axonal terminal are the mitochondria, which, together with other elements, create and store the neurotransmitter in muscle stimulation: acetylcholine.

Synaptic cleft:

The synaptic cleft is the area between the presynaptic bulb and the endplate of the motor.

In this contact area, the axonal structure’s terminal forms an extension placed in shallow subsidence of the fiber’s surface called the synaptic cleft.

The process by which neurotransmitters, such as acetylcholine, are released into the synaptic cleft is also known as the synapse.

Acetylcholine moves from the presynaptic membrane to the postsynaptic membrane by diffusion, acting later on the motor plate.

Engine plate:

When the axon enters the muscle, it branches into axonal terminals, and this region adjacent to these terminals, in the muscle fiber membrane, is called the motor plate.

The shape presented by the motor plate is that of a pit with folds, and this form is due to the need to adapt to the shape of the nerve terminal; thanks to these folds, it manages to increase its surface a lot.

The motor plate has some structures such as:

  • The synaptic channel is an invaginated membrane, which is the space for the synaptic bulbs to approach the sarcolemma of the muscle fiber.
  • The subneural slits: These are those small folds of the muscular membrane present in the lower area of ​​the synaptic channel. These slits significantly increase the size of ​​the surface on which the neurotransmitter can act.
  • Mitochondria: They are found in more significant numbers in the area of ​​the muscle fiber that is surrounding the endplate of the motor. The reason is that muscle cells are very active, and there is a great demand for energy in this neuromuscular junction.
  • Receptors: Many receivers are located on the motor endplate, with around 10,000 nicotinic receptors per square millimeter plate area. The acetylcholine that is released from the presynaptic bulbs binds nicotinic receptors.


Synapses and neuromuscular junctions are physiologically similar processes. However, the neuromuscular junction is a specific synapse between the motor neuron and the muscle fiber.

As it happens in a neuronal synapse, the arrival of an action potential to the axonic terminal gives rise to the opening of Ca2 channels.

The Ca ++ introduced in the neuron achieves that the synaptic vesicles adhere to the cell wall and release acetylcholine.

Then acetylcholine binds to these nicotinic receptors in the sarcolemma, the ion channels are opened, the sodium ions enter, and the calcium ions come out.

This positive charge of sodium and calcium ions causes neurons to change, transmitting electrical signals called action potentials.

Then the sarcoplasmic reticulum is activated, releasing the calcium ions stored in it.

Once the calcium ions have been released, the contraction of the myofibrils begins, as these ions diffuse between the protein filaments of actin and myosin.

In this way, the nerve impulse can spread through the muscle fiber and later to the whole muscle, eventually contracting it.

Thus, the neuromuscular junction is a connection or synapse between the somatic motor neuron and the muscle fiber, where the transformation of a chemical impulse to an electrical stimulation causes the contraction of the muscle fiber.

Diseases that affect the neuromuscular junction

Neuromuscular diseases represent a group of diseases of the hereditary origin that can be acquired and affect the muscle, the neuromuscular junction, the peripheral nerve, or the motor neuron.

Neuromuscular diseases have homogeneous clinical symptomatology in common, mainly determined by the presence of weakness, accompanied by atrophy or muscular pseudohypertrophy.

Difficulties to relax the muscle once a contraction has been performed, symptoms such as cramps or muscle contractures, myalgia, and sensory disorders.

Some of these diseases are affected by the neuromuscular junction and jeopardize the endplate of the motor and the motor neuron.

The motor neurons are responsible for processing and transferring information from the brain to the rest of the body and vice versa through nerve endings such as the motor plate.

Motor neuron diseases are a group of neurological disorders that are progressive and that destroy the motor neurons, producing decontrol in the essential voluntary muscular activity.

This type of disease treatment includes measures aimed at treating the defect in neuromuscular transmission in those myasthenic syndromes.

Also, to reduce axonal self-excitability and pathogenic, mainly immunosuppression.

Among these diseases can be cited:

Myasthenia gravis:

People who develop this disease suffer from progressive muscle weakness, where minimal activity can cause fatigue.

This disease is caused by the erroneous formation of autoantibodies against the nicotinic cholinergic receptors in the postsynaptic membrane, which does not allow the occurrence of neurotransmission.

In the treatment, drugs are used that will act on the inhibiting enzyme of acetylcholinesterase, causing an increase in the amount of acetylcholine.

Myasthenia gravis neonatal:

Neonatal myasthenia gravis occurs in newborns of mothers who have myasthenia gravis.

This condition is produced when the antibodies that block the nicotinic receptors are transferred from the mother to the fetus through the placenta.

Lambert-Eaton syndrome:

This disease causes autoantibodies to form against the calcium channels, so the flow of calcium ions will not occur, and therefore, neurotransmission will not happen.


Neuromyotonia, also known as the Isaac-Mertens syndrome, is a sporadic neuromuscular disorder caused by the continuous activation and hyperexcitability of axons of the peripheral nerves, whose function is to activate muscle fibers.

Duchenne muscular dystrophy:

Duchenne muscular dystrophy is a disease characterized by atrophy and progressive muscle weakness due to degeneration of the skeletal, smooth, and cardiac muscles.

This genetic disease causes the muscles to lose their functions progressively.

This loss of muscle functionality decreases the patient’s quality of life, and the life expectancy of this pathology does not exceed 30 years.

The disease is caused by a mutation in the gene responsible for coding dystrophin, an essential protein for muscles; the absence of the protein causes muscle cells to be damaged.

Bulbospinal muscular atrophy:

Bulbospinal muscular atrophy, or Kennedy’s disease, causes muscular atrophy due to motor neuron degeneration.

It is associated with the X chromosome.

It decreases the binding capacity of androgens and receptors, causing progressive paralysis.