PT  - JOURNAL ARTICLE
AU  - Henry J. Kaminski
AU  - Jose I. Suarez
AU  - Robert L. Ruff
TI  - Neuromuscular junction physiology in myasthenia gravis
AID  - 10.1212/WNL.48.Suppl_5.8S
DP  - 1997 Apr 01
TA  - Neurology
PG  - 8S--17S
VI  - 48
IP  - Suppl 5
4099  - http://n.neurology.org/content/48/Suppl_5/8S.short
4100  - http://n.neurology.org/content/48/Suppl_5/8S.full
SO  - Neurology1997 Apr 01; 48
AB  - Article abstract-The mammalian neuromuscular junction is a chemical synapse that uses acetylcholine as transmitter. Acetylcholine (ACh) is stored in the nerve terminal and is released from small membrane-bound vesicles that fuse with the nerve terminal membrane after depolarization of the nerve terminal. Calcium entry via P/Q-type calcium channels is necessary for transmitter release. The postsynaptic membrane of the muscle fiber has several unique properties that facilitate neuromuscular transmission. The postsynaptic membrane area is greatly expanded by synaptic folds. Acetylcholine receptors (AChR) are concentrated at the peaks of synaptic folds and sodium channels are concentrated in the troughs of the synaptic folds. The safety factor for neuromuscular transmission results from a combination of factors: the amount of ACh released, the high concentration of AChR, and the high concentration of sodium channels. AChR are firmly anchored in the membrane by a complex of proteins. The autoimmune attack in myasthenia gravis (MG) directed at acetylcholine receptors results in loss of postsynaptic membrane, AChR, and sodium channels. This article describes the different types of neuromuscular junctions on extraocular muscle fibers and their possible relevance to the susceptibility of extraocular muscle to MG. NEUROLOGY 1997;48(Suppl 5): S8-S17