Abstract
The muscarinic ganglion stimulating agent, McN-A-343 has unusual blocking actions on endplate currents (EPCs) at frog neuromuscular junctions. McN-A-343 caused depolarization by a curaresensitive process, blocked neuromuscular transmission, depressed EPCs and reduced the time for EPC decay. These results are explained best by a nicotinic agonist action of McN-A-343 on the acetylcholine receptor to cause ion flow and the blockade by McN-A-343 of the open ion channels. The actions of McN-A-343 are similar to those of decamethonium (C-10) described by others. Unlike C-10, however, McN-A-343 did not alter the exponential character of the EPC or alter the voltage dependency of the EPC. The prototypical nicotinic agonist, dimethylphenylpiperazinium had no effect on EPC parameters of endplate clamped at-90 mV.
Original language | English |
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Pages (from-to) | 117-121 |
Number of pages | 5 |
Journal | Naunyn-Schmiedeberg's Archives of Pharmacology |
Volume | 312 |
Issue number | 2 |
DOIs | |
Publication status | Published - Jun 1980 |
Keywords
- Depolarization blockade
- Endplate currents
- Ion channels
- McN-A-343
- Neuromuscular blockade
ASJC Scopus subject areas
- Pharmacology