Motorized end plate

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A motor end plate , also muscle end , neuromuscular junction , neuromuscular junction , myoneural Synapse , anatomically Terminatio neuromuscularis or Junctio neuromuscularis or synapsis neuromuscularis called, transmits the excitation of an efferent nerve fibers to the muscle of a skeletal muscle . Acetylcholine acts as a neurotransmitter for the transmission of excitation at this chemical synapse .

The transmission of excitation from a nerve cell to a muscle cell takes place at the neuromuscular endplate . The presynaptic terminal of the axon releases the neurotransmitter acetylcholine from synaptic vesicles .
Electron microscope image of a neuromuscular endplate in cross section - between the axon terminals (T) and muscle fibers (M) the synpatic gap with the basal lamina (arrow)

The neuromuscular synaptic connection consists of the presynaptic part of the axolemma of a nerve cell and the postsynaptic part of the sarcolemma of a muscle cell , separated by a synaptic gap with fine-fiber basal lamina . When the nerve cell is excited , the presynaptic terminal of the axon releases the messenger substance acetylcholine (ACh), which is distributed in the synaptic gap and reaches specific receptor molecules (ACh receptors) in the postsynaptic membrane region of a muscle fiber. Its surface is enlarged here by a multitude of folds (subneural folds).

Action potentials of an excited motor neuron are its axon (A) directed to the presynaptic Endknöpfchen (B) as part of a motor end plate - and can then several steps contractions of the associated muscle fiber lead

Action potentials arriving at the presynaptic part of the synapse cause the temporary opening of voltage-controlled calcium channels. The inflowing calcium (Ca 2+ ) acts as a signal in the synaptic terminal button and causes synaptic vesicles that contain acetylcholine to be mobilized. These move in the direction of the synaptic gap to the presynaptic membrane region of the terminal button. Vesicles that are already docked on the membrane fuse with it ( vesicle fusion ) and release the neurotransmitter acetylcholine into the synaptic gap ( exocytosis ). Acetylcholine binds to ionotropic acetylcholine receptors in the postsynaptic membrane of the muscle cell, which opens the ion channels of these receptors.

The ionotropic acetylcholine receptor is also known as the nicotinic acetylcholine receptor and is a non-specific cation channel that is conductive for sodium, calcium and potassium ions. It consists of five sub-units arranged around a central channel. Because of the prevailing concentration differences and the resulting driving forces for these ions, a current carried by sodium ions mainly flows through this channel into the cell. The result is a local depolarization of the muscle cell, the so-called end plate potential . This change in membrane potential, which deviates from the resting membrane potential, initially spreads electrotonically across the cell membrane; If the threshold potential in the neighboring sarcolemma is exceeded, voltage-controlled sodium channels open here, so that an action potential of the muscle cell is formed. This action potential then covers the entire cell membrane with all its folds and finally triggers the muscle contraction via subsequent calcium ion currents :

The opening of voltage-activated calcium channels in the transverse tubules of the muscle cell and the activation of intracellular ryanodine receptors (RYR1) lead to the release of calcium ions from the endoplasmic reticulum of the muscle cell. The sarcoplasmic reticulum stores calcium ions and forms a self-contained system of chambers that run primarily along the muscle fibrils ( longitudinal tubules ); from this, Ca 2+ can quickly be released in considerable quantities to the cytosol and reach every sarcomere of the fibrils. There, as a result of the strong increase in calcium concentration, binding sites for the motor protein myosin on the actin filaments are released, thereby triggering shifts in the myofilaments , which causes the myofibrils to shorten, which causes the muscle fibers to contract. Calcium ions thus play a key role in the electromechanical coupling .

The unbound acetylcholine in the synaptic cleft is broken down by the enzyme acetylcholinesterase and hydrolyzed to choline and acetate . In this way the effect of the emitted transmitter quanta is limited and ended. Choline can be taken up and reused by the presynaptic membrane region. The protein molecules of acetylcholinesterase are predominantly anchored to the basal lamina of the synaptic cleft.

If the function of the acetylcholine receptors z. B. is disturbed by autoimmune antibodies, it can lead to muscular fatigue and weakness ( myasthenia gravis ).

See also

Individual evidence

  1. ↑ a b Terminologia histologica , entry under H2.00.06.1.02001