Acetylcholine receptors (AChR) are organized in a discrete and predictable fashion in the postsynaptic regions of vertebrate skeletal muscle . When muscle is damaged, nerves and myofibers including muscular elements of the endplate degenerate, but the connective tissue elements survive. Muscle fibers regenerate within the basal lamina of the original myofiber . Postsynaptic differentiation in regenerated mammalian skeletal muscle can occur in different ways : (a) at the site of the original endplate in the presence or absence of the nerve, or (b) at ectopic regions of the regenerated myofiber in the presence of the nerve when the original endplate is not present. The present study used '251-a-bungarotoxin (1251 -a-BuTX) and EM autoradiography to examine the density and distribution of AChR in postsynaptic structures regenerated at the site of the original endplate in the absence of the nerve and at ectopic sites of the myofiber in the presence of the nerve when the original endplate was removed . In regenerated myofibers, the density of a-BuTX-binding sites fell within the range of densities observed in uninjured muscle whether postsynaptic differentiation occurred at the site of the original endplate in the absence of the nerve or at an originally ectopic position of the regenerated myofiber . In addition, the distribution of a-BuTX-binding sites within the regenerated postsynaptic regions closely resembled the distribution of a-BuTX-binding sites in uninjured muscle . Morphometric analysis was performed on postsynaptic structures formed at the site of the original endplate in the absence of the nerve or at an ectopic position of the regenerated myofiber by interaction of the nerve and muscle . Although variation in the depth of the primary cleft occurred, there was little difference between the overall structure of regenerated postsynaptic structures and that of endplates of uninjured muscles.The density of acetylcholine receptors (AChR) at innervated motor endplates of skeletal muscle has been determined by both physiological (23, 25) and morphological (16,28,30,(33)(34)(35) means. Various studies (for review see reference 12) have shown that the number of AChR at endplates in mice (2), rats (14, 31), frogs (31), and humans (13) is quite similar. Electron microscope autoradiographic studies have demonstrated a relatively constant density (16,28,30,(33)(34)(35) and distribution (16,(33)(34)(35) of AChR at endplates of vertebrate skeletal muscle .When skeletal muscle grafts are made, the neuromuscular junctions are disrupted by the degeneration of the myofibers and the nerves that supply them (7,10,29,37, and footnote 1).' Carlson, B. M., P. Hnik, S. Tucek, R. Vejsada, and D. Bader.
338It has been established that synapses are formed in the regenerated muscle of amphibians (29, 37) and mammals (1,3,10). Marshall et al . (29) have shown that, in regenerating frog muscle, neuromuscular connections are almost always at the site of the original endplate . Burden et al . (7) have demonstrated that postsyna...