Postsynaptic block of frog neuromuscular transmission by conotoxin GI.

摘要: Conotoxin GI, a peptide neurotoxin contained in the venom of marine snail Conus geographus, was applied to cutaneous pectoris muscle frog, and effects on postsynaptic response acetylcholine were examined. GI reversibly blocked nerve-evoked contractions at concentrations greater than or equal 3 4 microM. Micromolar conotoxin significantly reduced amplitude miniature endplate potentials membrane depolarizations produced by ionophoretic application acetylcholine, suggesting that toxin sensitivity acetylcholine. The reduction not due changes fiber resting potential input resistance. amplitudes but did affect rates decay focal, extracellularly recorded currents currents, lifetime ion channels opened Miniature five six times more slowly normal when acetylcholinesterase is with neostigmine methyl sulfate repeated binding receptors as it diffuses from synaptic cleft. increased rate presence sulfate, receptors. These results are consistent hypothesis blocks neuromuscular transmission frog reducing