AbstractThe 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 exposedin vitroto acetylcholine (10−3g/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‐amino‐phenoxylethane‐N,N1;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+entr
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