BAY K 8644 increases release of acetylcholine at the murine neuromuscular junction.

In this study we describe the stimulatory effects of submicromolar concentrations of BAY K 8644 on neurally evoked and spontaneous release of transmitter at the vertebrate neuromuscular junction, a model cholinergic synapse. BAY K 8644 increases mean quantal content. This effect is blocked by pretreatment with the dihydropyridine (DHP) antagonist, nimodipine, but nimodipine itself had no effect on quantal content. Furthermore, BAY K 8644 induces a marked increase in spontaneous quantal release of transmitter as measured by miniature endplate potential frequency. These results are important in that they indicate that DHP-sensitive Ca2+ channels exist at motor nerve terminals and when activated can participate in transmitter release; second, they imply that these elements do not normally participate in transmitter release; third, they indicate a functional effect of DHPs on neurons under somewhat more relevant physiological conditions than those imposed by prolonged K+-induced depolarization, a technique used to evoke transmitter release in subcellular systems and fourth, they indicate an effect of BAY K 8644 on spontaneous release of transmitter, an effect not reported in previous neurochemical experiments.