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.
D000818:Animals; D001030:Apamin / Q000494:pharmacology*; D001514:Bee Venoms / Q000494:pharmacology*; D002415:Cats; D004553:Electric Conductivity; D005260:Female; D007473:Ion Channels / Q000187:drug effects; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009046:Motor Neurons / Q000187:drug effects*; D011188:Potassium / Q000378:metabolism; D013116:Spinal Cord / Q000187:drug effects*
D001514:Bee Venoms; D007473:Ion Channels; D001030:Apamin; D011188:Potassium