A comparison of nerve transection and chronic application of beta-bungarotoxin on acetylcholine receptor distribution and other nerve-muscle properties.

beta-Bungarotoxin (beta-BuTX), a snake venom neurotoxin which acts presynaptically to inhibit acetylcholine (ACh) release at the neuromuscular junction, was applied to the rat phrenic nerve-diaphragm muscle preparation to determine its effectiveness to mimic denervation. The distribution of junctional and extrajunctional ACh receptors on the muscle were assayed biochemically by [125I]alpha-bungarotoxin ( [125I]alpha-BuTX) binding and electrophysiologically by iontophoretic application of ACh. Spontaneous transmitter release and muscle membrane potential were measured under conditions of denervation, beta-BuTX treatment, and bee venom phospholipase A2 exposure. Within 7 days after treatment with a single dose (5 micrograms/kg) of enzymatically active beta-BuTX, extrajunctional [125I]alpha-BuTX binding increased fivefold, and there was a decrease in miniature end-plate potential (MEPP) frequency and in resting membrane potential (RMP) to values less than those of control muscles but greater than those of denervated.