The motor or neuromuscular endplate, is the point of contact between a motor neuron and a muscle cell. It is also called the neuromuscular synapse and is used to transmit excitation between a motor nerve fiber and a muscle fiber.
What is the motor end plate?
The neuromuscular synapse is an excitatory synapse that specializes in the chemical transmission of peripheral nerve stimuli to excite skeletal muscle. The nerve terminal of the motoneuron and the muscle cell are connected by a plate-like widened contact site. This acts as a transmission site for electrical impulses arriving from the peripheral nervous system. However, the motor nerve fiber and the muscle fiber it innervates are separated by a narrow space. Thus, there is no direct point of contact. For the transmission of excitation, therefore, the electrical impulses are converted into chemical stimuli. Certain chemical messengers, so-called neurotransmitters, are used for this purpose. In response to the excitation received at the motor endplate, the neurotransmitter acteylcholine is released, which transmits the signal to the muscle cell according to the one-way principle, triggering contraction of the triggered muscles.
Anatomy and structure
A nerve cell is essentially composed of a cell body and a long nerve extension, the axon. The cell body receives excitation via dendrites, short extension-like branches, which the axon carries away. The thickened end of the axon is called the synaptic terminal button and lies almost, i.e. without direct contact, on the controlled muscle cell. The motor end plate is to be understood as a functional unit for the transmission of excitation and is roughly composed of three parts. The presynaptic membrane belongs to the motor neuron and includes the synaptic terminal button with a supply of the neurotransmitter acteylcholine packed in small vesicles. In addition, voltage-gated calcium channels are embedded in the membrane. The postsynaptic membrane corresponds to the muscle fiber membrane and has acetylcholine receptors coupled to ion channels for sodium and potassium that cause them to open by binding the neurotransmitter. Between the presynaptic and postsynaptic membranes is the synaptic cleft, which is largely enriched in water molecules but also contains ions (e.g., sodium, chloride, and calcium) and enzymes to break down acetylcholine.
Function and tasks
The neuromuscular endplate enables the specific control and contraction of skeletal muscles through chemical stimulus transmission. Once excitation, or action potential, arrives at the synapse, voltage-gated calcium channels in the presynaptic membrane open. The incoming calcium binds to the neurotransmitter-filled vesicles and causes them to fuse with the presynaptic membrane. The acetylcholine is thus released outward into the synaptic cleft and diffuses to the postsynaptic muscle fiber membrane. There it binds to the acetylcholine receptors, leading to the opening of the sodium and potassium channels. The resulting strong influx of sodium ions with a simultaneous weak outflow of potassium ions depolarizes the postsynaptic membrane potential. A so-called end-plate potential is generated, which triggers an action potential in the muscle cell when a certain threshold value is exceeded. The propagating action potential induces the release of calcium from the sarcoplasmic reticulum via voltage-gated ion channels. The released calcium then activates the sliding mechanism of the muscle fiber filaments actin and myosin. As these filaments slide into each other, the muscle shortens and contraction occurs. After successful transmission of excitation, acetylcholine is cleaved from the receptor. Via the enzyme cholinesterase, the neurotransmitter is broken down into acetate and choline and the individual building blocks are reabsorbed into the presynaptic cell, where they are synthesized again to acetylcholine and then packaged into vesicles.
Diseases
Diseases affecting the motor endplate are referred to as disorders of neuromuscular excitation transmission because the connection between the nerve and muscle, and therefore the transmission of stimuli, is damaged.The disorders primarily comprise various myasthenia syndromes that are associated with varying degrees of strain-dependent muscle weakness. As a rule, the symptoms increase during the course of the day and with fatigue, exertion or external stress factors such as stress, whereas they improve during periods of relaxation. The various forms of myasthenic disorders are generally characterized by a rather atypical clinical picture with individual impairments and an individual course. Myasthenia gravis is an autoimmune disease in which antibodies at the motor endplate block the acetylcholine receptors of the postsynaptic membrane. In the common generalized form, muscle weakness can spread to the entire skeletal musculature and even become life-threatening if respiratory muscle function is impaired. Lambert-Eaten syndrome (LES) is also an autoimmune disease. However, the impaired excitation transmission manifests itself at the synaptic terminal. The antibodies block the calcium channels at the presynaptic membrane, resulting in impaired release of the neurotransmitter actelycholine. Typical symptoms include delayed maximal force development and rapid muscle fatigue, especially proximally and near the trunk. LES usually occurs in association with tumors. However, myasthenic syndromes can also accompany endocrine disorders such as diabetes mellitus or hyperthyroidism. In these cases, the symptoms usually subside as soon as the underlying disease is treated. However, there are also congenital disorders resulting from genetic defects. Complaints such as muscle weakness or paralysis can also be caused by nerve toxins. For example, the highly toxic botulinus toxin inhibits the release of the neurotransmitter acetylcholine at the neuromuscular end plate and has a lethal effect even in low doses.
