Acetylcholinesterase in the neuromuscular junction

New findings regarding acetylcholinesterase (AChE) in the neuromuscular jun ction (NMJ), obtained in the last decade,are briefly reviewed. AChE is high ly concentrated in the NMJs of vertebrates. Its location remains stable aft er denervation in mature rat muscles but not in early postnatal muscles. Ag rin in the synaptic basal lamina is able to induce sarcolemmal differentiat ions accumulating AChE even in the absence of a nerve ending. Asymmetric A( 12) AChE form is the major molecular form of AChE in vertebrate NMJs. Extra junctional suppression of this form is a developmental phenomenon. Motor ne rve is able to reinduce expression of the A(12) AChE form in the ectopic NM Js even in muscles with complete extrajunctional suppression of this form. The 'tail' of the A(12) AChE form. is made of collagen Q. It contains domai ns for binding AChE to basal lamina with ionic and covalent interactions. M uscle activity is required for normal AChE expression in muscles and its ac cumulation in the NMJs. In addition, the pattern of muscle activation also regulates AChE activity in the NMJs, demonstrating that the pattern of syna ptic transmission is able to modulate one of the key synaptic components. ( C) 1999 Elsevier Science Ireland Ltd. All rights reserved.