The role of Ca2+ in the elimination of polyneuronal innervation of rat soleus muscle fibres.

The mechanism by which nerve - muscle contacts are reduced during postnatal development of the rat soleus muscle was investigated using electrophysiological methods. Between days 7 and 9 after birth, soleus muscle fibres lose 0.19 - 0.24 terminals per muscle fibre within 24 h. A much more rapid loss of contacts is seen when muscles are exposed in vitro to acetylcholine (10-3 g/ml). In this case 0.67 - 0.87 terminals per muscle fibre lose contact within 2 h. The loss of neuromuscular contacts induced by acetylcholine can be reduced by preincubating the muscles in solutions containing acetoxymethyl ester of 1,2-bis(2-aminophenoxylethane-N,N1,N;N1-tetraacetic acid (BAPTA-AM), a Ca2+ chelating agent that enters cells and reduces the Ca2+ transients inside the cell. Treatment of muscles with nifedipine, which blocks dihydropyridine-sensitive (L-type) Ca2+ channels, also reduced the acetylcholinesterase-induced loss of neuromuscular contacts. The results indicate that transient increases in Ca2+ inside nerve terminals contribute to loss of neuromuscular contacts, and that these increases occur by Ca2+ entry through L-type channels.