Definition
The motor endplate (neuromuscular endplate) is a chemical synapse that can transmit electrical excitation from the end of a nerve cell to a muscle fiber.
Task of the motorized end plate
The task of the motor end plate is to transmit excitation, i.e. an action potential that has been conducted through the nerve fiber, from the latter to the muscle cell, thus enabling the muscle to contract (contract).
Structure
The motorized end plate usually consists of three parts:
- The end button of the nerve fiber, which represents a widening at the end of the axon of this fiber, or the membrane present here, which is also called the presynaptic membrane (= membrane located in front of the synapse),
- The opposite part of the membrane of the muscle fiber cell, which is also called the postsynaptic membrane (= membrane after the synapse) and
- The synaptic gap located between the two membranes.
Procedure of an excitation
When an action potential reaches the end button of the nerve cell, voltage-controlled calcium channels open in the membrane of this end button. The calcium ions then flow into the cell and bind to small vesicles in the cytoplasm, which are filled with the transmitter acetylcholine. As the calcium ions are now bound to the vesicles, they are induced to move towards the presynaptic membrane and fuse with it.
This process is known as exocytosis and results in the contents of the vesicles, in this case acetylcholine, being emptied to the outside. It is now located in the synaptic cleft. The postsynaptic membrane is equipped with a multitude of receptors for this neurotransmitter.
These receptors are called ionotropic, because they are linked to an ion channel that opens after the receptors are occupied. The acetylcholine receptors that occur here are nicotinic acetylcholine receptors, a term that comes from the fact that the substance nicotine can also dock to these receptors (although the concentration of nicotine that is reached by smoking, for example, is not sufficient to open the channels). In addition, there is another receptor for acetylcholine, called the muscarinic acetylcholine receptor, which does not occur on muscle cells but in the parasympathetic nervous system.
When acetylcholine binds to the nicotinic receptor, a channel opens up that is permeable for cations (i.e. positively charged ions). Due to the concentration of these ions inside and outside of the muscle cell and the resulting driving forces, this leads to a flow of mainly sodium ions and calcium ions into the muscle fiber. As a consequence, the end plate potential of the postsynaptic membrane becomes more and more positive, one speaks of a depolarization of the cell.
Thus, the so-called resting potential of the cell first becomes a generator potential, which spreads passively along the muscle fiber electrotonically. However, if a certain threshold value is exceeded, voltage-dependent sodium channels also open up. This process causes the creation of an action potential which can spread much faster.
Via the membrane, the action potential also reaches the tubule system of the muscle cell. Here, voltage-controlled calcium channels are opened due to the incoming action potential, which activates the ryanodine receptors of the sarcoplasmic reticulum (which corresponds to the endoplasmic reticulum of somatic cells). The result is that a massive release of calcium ions now occurs from this reservoir.
The calcium in turn ensures that the binding site of actin and myosin is released, thereby initiating the sliding filament mechanism: The muscle fiber shortens and the muscle contracts. This process is also known as electromechanical coupling, since an originally electrical signal (namely the action potential) leads to a mechanical reaction (namely the contraction of the muscle). The acetylcholine, which was previously released into the synaptic cleft, cannot return as such to the end button of the nerve cell.
Therefore, an enzyme, acetylcholinesterase, splits it first into its components acetate and choline, which can migrate separately through the presynaptic membrane, unite and are now repackaged into vesicles as acetylcholine.Among other things, the concentration of acetylcholinesterase in the synaptic cleft allows the length and intensity of muscle contraction to be controlled, as it directly affects how long the acetylcholine remains there and can cause contraction. This is why it is the point of attack of some drugs as well as some poisons.
