五氯苯酚（PCP）对蟾蜍神经肌肉接头的影响。

The effects of pentachlorophenol (PCP) at the toad neuromuscular junction.

Montoya G A, Quevedo L

Department of Physiological Sciences, Faculty of Biological Sciences and Natural Resources, University of Concepción, Chile.

Comp Biochem Physiol C Comp Pharmacol Toxicol. 1990;96(1):193-7. doi: 10.1016/0742-8413(90)90067-j.

Abstract

Effects of PCP at the frog neuromuscular junction were studied in vitro in sciatic nerve sartorius muscle of the toad Pleurodema-thaul. 2. Within the concentration 0.003-0.1 mM, PCP caused a dose-time-dependent block of evoked transmitter release acompanied by an increase in the rate of spontaneous quantal release. 3. PCP induced an increase in miniature endplate potential (MEPP) frequency and it was not antagonized in a Ca2(+)-free medium, indicating that it does not depend upon Ca2+ influx from the external medium, but may act by releasing Ca2+ from intraterminal stores. 4. The present data, together with previous results concerning PCP at eighth sympathetic ganglia indicate that 3,4-diaminopyridine (3,4-DAP) counteracts the effects of PCP on synaptic transmission. This result suggests that PCP interfering Ca2+ influx occurs during depolarization of motor nerve terminals.

摘要

在体外对蟾蜍侧褶蛙的坐骨神经缝匠肌进行研究，以探讨苯环己哌啶（PCP）对青蛙神经肌肉接头的影响。2. 在0.003 - 0.1 mM的浓度范围内，PCP引起诱发递质释放的剂量 - 时间依赖性阻滞，并伴有自发量子释放速率的增加。3. PCP诱导微小终板电位（MEPP）频率增加，且在无Ca2+的培养基中未被拮抗，这表明它不依赖于细胞外介质中的Ca2+内流，而是可能通过从终末内储存库释放Ca2+起作用。4. 目前的数据，连同先前关于PCP对第八交感神经节作用的结果表明，3,4 - 二氨基吡啶（3,4 - DAP）可抵消PCP对突触传递的影响。这一结果表明，PCP干扰Ca2+内流发生在运动神经末梢去极化期间。