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The Role of Ca 2+ in the Elimination of Polyneuronal Innervation of Rat Soleus Muscle Fibres
Author(s) -
Zhu PeiHong,
Vrbová G.
Publication year - 1992
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1992.tb00893.x
Subject(s) - soleus muscle , neuromuscular junction , chemistry , neuromuscular transmission , biophysics , acetylcholine , nifedipine , dihydropyridine , calcium , bapta , electrophysiology , anatomy , medicine , skeletal muscle , biology , neuroscience , organic chemistry
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‐amino‐phenoxylethane‐N,N 1 ;N 1 ‐tetraacetic acid (BAPTA‐AM), a Ca 2+ chelating agent that enters cells and reduces the Ca 2+ transients inside the cell. Treatment of muscles with nifedipine, which blocks dihydropyridine‐sensitive (L‐type) Ca 2+ channels, also reduced the acetylcholinesterase‐induced loss of neuromuscular contacts. The results indicate that transient increases in Ca 2+ inside nerve terminals contribute to loss of neuromuscular contacts, and that these increases occur by Ca 2+ entry through L‐type channels.