CALCIUM INFLUX THROUGH N-TYPE AND P Q-TYPE CHANNELS ACTIVATE APAMIN-SENSITIVE CALCIUM-DEPENDENT POTASSIUM CHANNELS GENERATING THE LATE AFTERHYPERPOLARIZATION IN LAMPREY SPINAL NEURONS/

Lamprey spinal neurons exhibit a fast afterhyperpoiarization and a lat e afterhyperpolarization (AHP) which is due to the activation of apami n-sensitive SK Ca2+-dependent K+ channels (K-Ca) activated by calcium influx through voltage-dependent channels during the action potential (Hill et al. 1992, Neuroreport, 3, 943-945). In this study we have inv estigated which calcium channel subtypes are responsible for the activ ation of the K-Ca channels underlying the AHP. The effects of applying specific calcium channel blockers and agonists were analysed with reg ard to their effects on the AHP. Blockade of N-type calcium channels b y omega-conotoxin GVIA resulted in a significant decrease in the ampli tude of the AHP by 76.2 +/- 14.9% (mean +/- SD). Application of the P/ Q-type calcium channel blocker: omega-agatoxin IVA reduced the amplitu de of the AHP by 20.3 +/- 10.4%. The amplitude of the AHP was unchange d during application of the L-type calcium channel antagonist nimodipi ne or the agonist (+/-)-BAY K 8644, as was the compound afterhyperpola rization after a train of 10 spikes at 100 Hz. The effects of calcium channel blockers were also tested on the spike frequency adaptation du ring a train of action potentials induced by a 100-200 ms depolarizing pulse. The N- and P/Q-type calcium channel antagonists decreased the spike frequency adaptation, whereas blockade of L-type channels had no effect. Thus in lamprey spinal cord motor- and interneurons, apamin-s ensitive K-Ca channels underlying the AHP are activated primarily by c alcium entering through N-type channels, and to a lesser extent throug h P/Q-type channels.