Effect of beta-agkistrodotoxin (beta-AgTx), a presynaptic neurotoxin purified from snake venom, on large-conductance calcium-activated potassium channels (BK(Ca)) was studied in rat hippocampal CA1 pyramidal neurons using inside-out configuration of patch-clamp technique. The results showed that in equimolar K+ (150 mM) and 1 microM intracellular Ca2+ conditions, internal application of beta-AgTx inhibited the activity of BK(Ca) by reducing open probability (P(o)) of the channels in a concentration-dependent manner. High concentration (74 nM) of beta-AgTx completely eliminated opening of the channels. However, 37 nM beta-AgTx (at -40 mV) decreased P(o) from 0.49+/-0.07 to 0.03+/-0.03, switched two open time constants (0.51+/-0.32 and 8.77+/-1.63 ms) to be a single time constant of 0.46+/-0.40 ms. The results indicate that inhibition of BK(Ca) by beta-AgTx may account for the facilitatory phase of the toxin on acetylcholine release from nerve terminals.
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