DISASSEMBLY OF THE CHOLINERGIC POSTSYNAPTIC APPARATUS INDUCED BY AXOTOMY IN MOUSE SYMPATHETIC NEURONS - THE LOSS OF DYSTROPHIN AND BETA-DYSTROGLYCAN IMMUNOREACTIVITY PRECEDES THAT OF THE ACETYLCHOLINE-RECEPTOR

In mouse sympathetic superior cervical ganglion (SCG), cortical cytosk eletal proteins such as dystrophin (Dys) and beta 1 Sigma 2 spectrin c olocalize with beta-dystoglycan (beta-DG), a transmembrane dystrophin- associated protein, and the acetylcholine receptor (AChR) at the posts ynaptic specialization. The function of the dystrophin-dystloglycan co mplex in the organization of the neuronal cholinergic postsynaptic app aratus was studied following changes in the immunoreactivity of these proteins during the disassembly and subsequent reassembly of the posts ynaptic specializations induced by axotomy of the ganglionic neurons. After axotomy, a decrease in the number of inh aganglionic synapses wa s observed (t1/2 8 h 45'), preceded by a rapid decline of postsynaptic specializations immunopositive for beta-DG, Dys, and alpha 3 AChR sub unit alpha 3AChR (t1/2 3 h 45', 4 h 30' and 6 h, respectively). In con trast, the percentage of postsynaptic densities immunopositive for bet a 1 Sigma 2 spectrin remained unaltered. When the axotomized neurons b egan to regenerate their axons, the number of intraganglionic synapses increased,as did that of postsynaptic specializations immunopositive for beta-DG, Dys, and alpha 3AChR. The latter number increased more sl owly than that of Dys and beta-DG. These observations suggest that in SCG neurons, the dystrophin-dystroglycan complex might play a role in the assembly-disassembly of the postsynaptic apparatus, and is probabl y involved in the stabilization of AChR clusters.