1. 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. © 1990.
Montoya, G. A., & Quevedo, L. (1990). The effects of pentachlorophenol (PCP) at the toad neuromuscular junction. Comparative Biochemistry and Physiology. Part C, Comparative, 96(1), 193–197. https://doi.org/10.1016/0742-8413(90)90067-J