Acetylcholine receptor availability and transmission efficacy.

Recovery of cholinergic transmission after in vivo blockade with alpha-bungarotoxin (alpha-BTX), and the relationship of recovery to availability of unbound acetylcholine receptors (AChR) were studied in rat diaphragm. When 83% of endplate acetylcholine receptor binding sites were blocked, transmission was absent. A barely detectable recovery of the blocked receptors (25 h after exposure to alpha-bungarotoxin) restored transmission. In fact, 25% of the endplate receptor ACh binding sites were just sufficient for action potential generation. As discussed, slow turnover (t 1/2 = 11 days) of junctional receptors would be sufficient to provide the observed recovery of transmission. Good agreement was observed between the minimum fraction of total receptor sites required for transmission and the computed fraction of maximum quantal release of acetylcholine required to reach threshold. In addition, the data are consistent with the hypothesis that at the neuromuscular junction, AChR exists in considerable excess.