Apamin depresses selectively the after-hyperpolarization of cat spinal motoneurons.

Extra- (but not intra-) -cellularly applied apamin depresses selectively the after-hyperpolarization (AHP) of cat spinal motoneurons in situ, while causing only a slight depolarization and minor changes in size and shape of the action potential. Apamin increases firing evoked by long depolarizing current pulses. These results indicate that the Ca2+-dependent K conductance underlying the AHP is sensitive to apamin, and that this conductance is likely to have a physiological role in the control of motoneuronal firing.