Effects of charybdotoxin, a blocker of Ca2+-activated K+ channels, on motor nerve terminals.

1. The contribution of Ca2+-activated K+ currents (IK,Ca) to the control of electrical excitability of motor nerve terminals and the control of acetylcholine release was assessed by studying the effects of the specific K(Ca) channel blocking toxins charybdotoxin and apamin. Electrical activity of the terminal regions of motor nerves was assessed by extracellular recording from an electrode placed in the perineural sheaths of nerves in the mouse triangularis sterni and frog cutaneous pectoris preparations. Acetylcholine release was monitored by intracellular recording of endplate potentials (e.p.ps). 2. Charybdotoxin (20-300 nM), but not apamin (10 nM-2.5 microM), selectively reduced the amplitude of an IK,Ca unmasked by prior blockade of the delayed rectifier K+ current with 3,4-diaminopyridine (3,4-DAP). 3. In the combined presence of 3,4-DAP and charybdotoxin, large Ca2+-dependent plateau responses developed, but only moderate and transient increases in acetylcholine release occurred. 4. In the absence of 3,4-DAP, charybdotoxin did not alter the electrical activity of, or the transmitter release from motor nerve terminals. 5. A possible role of the charybdotoxin-sensitive IK,Ca in the control of transmitter release is discussed.