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of ACh, prolonging the duration of EPPs by allowing ion channels to remain open for longer periods of time and enhancing end-plate responsiveness to ACh468,477 480 The net effect is for reduced temperature to enhance NMT, which has both electrophysiological and clinical signi cance AChE exists in at least two isoforms: AChE-S and AChE-R (Fig 23 6) AChE-S plays a critical role in terminating the action of ACh on the AChR It is anchored on the basement membrane via its collagen tail Mutations of the AChE gene produce one form of congenital myasthenia Weakness in this disorder results from excessive depolarization in a manner similar to the effects of succinylcholine The AChE-R isoform differs from its S counterpart in that its levels are more variable and change in response to external in uences, and it is soluble as it lacks an anchoring domain Its function is apparently to limit ACh access to the AChR Overexpression of AChER impairs NMT443 Suppression of AChE-R synthesis may provide a novel means of treating DNMT481 There are two other forms of cholinesterase present in the synaptic cleft: butyryl cholinesterase (pseudocholinesterase) and eserin-resistant carboxylic esterase Neither is felt to play a role in the normal physiology of NMT453,471,482 484 Postjunctional folds are not well formed at birth but develop with age485 Their summits assume a perpendicular orientation to the synaptic cleft and presynaptic terminal (Fig 23 6) Generally, fast twitch muscle bers have more pronounced and extensive junctional folds than slow twitch muscle bers486 The summits of the junctional folds are thicker than the recesses due to the presence of small particles, 6 12 nm in diameter, with a spatial density reaching 10,000 particles/m2 The density of these membrane structures decrease by >95% as one proceeds into the recesses of the secondary synaptic clefts487 Alpha bungarotoxin speci cally and irreversibly binds to the AChR When this toxin is radiolabeled and exposed to NMJs, it demonstrates a very good geographic correlation between toxin and intramembranous particle location As a result, it is generally accepted that the AChR and above-noted particles are identical structures The topographical distribution of AChR and related proteins are integral components of normal NMT (Fig 23 7) The AChRs are anchored to the sarcolemma and induced to cluster by the protein rapsyn located in the immediate subsarcolemmal region Rapsyn is, in turn, bound to the transmembrane protein -dystroglycan, which is linked to the intracellular cytoskeleton by utrophin1,443,488 This complex is similar to the dystrophin glycoprotein complex In addition, The AChR utrophin glycoprotein complex is connected to the extracellular matrix by agrin, a basement membrane protein, which is also thought to be responsible for AChR aggregation Agrin colocalizes with MuSK and AChRs in the sarcolemmal membrane MuSK is thought to facil-.

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