Impaired neuromuscular transmission during partial inhibition of acetycholinest‐erase: The of stimulus‐induced antiromic backfiring in the generation of the decrement–increment phenomenon
Impaired neuromuscular transmission during partial inhibition of acetycholinest‐erase: The of stimulus‐induced antiromic backfiring in the generation of the decrement–increment phenomenon
复制标题
部分抑制乙酰胆碱酯酶期间神经肌肉传递受损:在递减-递增现象的产生中刺激诱导的逆转录反应
DOI:
10.1002/mus.880151003
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发表时间:
1992
期刊:
影响因子:
3.4
通讯作者:
I. Wessler
中科院分区:
文献类型:
--
作者:
R. Besser;T. Vogt;L. Gutmann;H. Hopf;I. Wessler
Neuromusuclar transmission was studied in the rat phrenic nerve–hemidiaphragm preparation with acetylcholinesterase (AChE) partially inactivated. Enzyme inhibition resulted in (1) increased single‐twitch tension of the diaphragm; (2) compound muscle action potential (CMAP) containing repetitive discharges; (3) stimulus‐induced antidromic backfiring (SIAB) seen in the phrenic nerve; and (4) repetitive nerve stimulation (RNS) eliciting a decrement—increment (D‐I) phenomenon (i.e., amplitude reduction maximal with the second CMAP). Using a high‐calcium and low‐magnesium solution, SIAB and the decrement of the second CMAP during RNS were intensified, whereas closely spaced trains and (+)‐tubocurarine (TC) abolished SIAB and simultaneously prevented the decrement of the second CMAP. Importantly, low concentrations of (+)‐TC prevented SIAB in the phrenic nerve, while the repetitive discharges of the CMAP and the increase in twitch tension remained unaffected. This observation suggests that preterminal nicotinic receptors stimulated by released acetylcholine induce SIAB, whereas postsynaptic events are less important in the generation of SIAB. SIAB, a presynaptic event, appears to be responsible for the transient impairment of the neuromuscular transmission, i.e., the D‐I phenomenon.