Modulation of burst frequency by calcium-dependent potassium channels in the lamprey locomotor system: dependence of the activity level.

It is crucial to determine the effects on the network level of a modulation of intrinsic membrane properties. The role calcium-dependent potassium channels, KCa, in the lamprey locomotor system has been investigated extensively. Earlier experimental studies have shown that apamin, which affects one type of KCa, increases the cycle duration of the locomotor network, due to effects on the burst termination. The effects of apamin were here larger when the network had a low level of activity (burst frequency 0.5 to 1 Hz) as compared to a higher rate (> 2 Hz). By using a previously developed simulation model based on the lamprey locomotor network, we show that the model could account for the frequency dependence of the apamin modulation, if only the KCa conductance activated by Ca2+ entering during the action potential was altered and not the KCa conductance activated by Ca2+ entering through NMDA channels. The present simulation model of the spinal network in the lamprey can thus account for earlier experimental results with apamin on the network and cellular level that previously appeared enigmatic.