Neuromuscular Junction - Structure - Neuromuscular Junction

The neuromuscular junction differs from synapses in the central nervous system. Presynaptic motor axons are demyelinated and stop 30 nanometers from the sarcolemma, the cell membrane of a muscle cell. This 30-nanometer space forms the synaptic cleft through which signaling molecules are released. The sarcolemma has invaginations called postjunctional folds, which increase the surface area of the membrane exposed to the synaptic cleft. These postjunctional folds form what is referred to as the motor end-plate, which possesses acetylcholine receptors (AChRs) at a density of 10,000 receptors/micrometer2 in skeletal muscle. The presynaptic axons form bulges called terminal boutons that project into the postjunctional folds of the sarcolemma. The presynaptic boutons have active zones that contain vesicles, quanta, full of acetylcholine molecules. These vesicles can fuse with the presynaptic membrane and release ACh molecules into the synaptic cleft via exocytosis after depolarization. AChRs are localized by protein scaffolds at the postjunctional folds of the sarcolemma opposite the presynaptic terminals. Dystrophin, a structural protein, connects the sarcomere, sarcolemma, and extracellular matrix components. Rapsyn is another protein that docks AChRs and structural proteins to the cytoskeleton. The receptor tyrosine kinase protein MuSK is a signaling protein involved in the development of the neuromuscular junction and is also held in place by rapsyn.

Read more about this topic:  Neuromuscular Junction, Structure

Other articles related to "neuromuscular junction, neuromuscular, neuromuscular junctions, junction":

Neuromuscular Junction - Toxins - Snake Venom
... Snake venoms can act as toxins within the neuromuscular junction by inducing the weakness and that occurs after a venomous snake bite ... known as β-neurotoxins, affect the presynaptic regions of the neuromuscular junction ... Those that inhibit neurotransmitter release create a neuromuscular blockade that prevents signaling molecules from reaching their postsynaptic target receptors ...
Thyrotoxic Myopathy - Pathophysiology
... specifically at the motor end plates of neuromuscular junctions ... can be toxic and lead to TM physiologically first consider basic neuromuscular junction function ... from the brain or spinal cord towards the neuromuscular junction ...
Neuromuscular Junction Disease
... Neuromuscular junction disease is a medical condition where the normal conduction through the neuromuscular junction fails to function correctly ...
Butyrylcholinesterase - Clinical Significance
... Of these, its most clinically important substrate is the depolarizing neuromuscular blocking agent, succinylcholine, which the pseudocholinesterase enzyme hydrolyzes to succinylmonocholine and then to ... of approximately 90-95% of an intravenous dose of succinylcholine occurs before it reaches the neuromuscular junction ... of the succinylcholine dose acts as an acetylcholine receptor agonist at the neuromuscular junction, causing prolonged depolarization of the postsynaptic junction of the motor-end ...
End-plate Potential - Clinical Applications
... the acetylcholine receptor on the postsynaptic membrane in the neuromuscular junction ... reduce the breakdown of acetycholine in the neuromuscular junction, so that enough acetylcholine will be present for the small number of unblocked receptors A ... It prevents release of acetylcholine at the neuromuscular junction by inhibiting docking of the neurotransmitter vesicles ...

Famous quotes containing the word junction:

    In order to get to East Russet you take the Vermont Central as far as Twitchell’s Falls and change there for Torpid River Junction, where a spur line takes you right into Gormley. At Gormley you are met by a buckboard which takes you back to Torpid River Junction again.
    Robert Benchley (1889–1945)