The Role of Voltage Dependent Calcium Channels in Identified Motoneurons During Fictive Locomotor Behavior

Abstract

The primary goal of this work was to examine the role of voltage-dependent Ca2+ channels in regulating the output of larval Drosophila motoneurons functioning within an intact network. To accomplish this goal, two major aims were addressed: 1. To determine whether larval Drosophila motoneurons express voltage-dependent Ca2+ channels in their central processes, and further, to determine the genes responsible. 2. To determine the role of centrally expressed voltage-dependent Ca2+ channels in the regulation of motoneuron output as motoneurons receive behaviorally relevant input from the locomotor network. To address these goals, genetic tools available in Drosophila were used along side in situ patch clamp techniques from larval motoneurons.Using whole cell voltage-clamp techniques in situ, we have shown that two identified motoneurons, aCC and RP-2, carry voltage-dependent currents recorded from the soma. Dmca1D, the L-type like channel in Drosophila, is primarily responsible for this current. Expressing Dmca1D RNAi in aCC and RP-2, as the preparation displayed fictive bouts of locomotion, caused an increase in burst duration in both RP-2 and aCC as well as an increase in the number of action potentials fired per burst. Additionally, the afterhyperpolarization between spikes was greatly reduced and spiking became less regular. This work indicates a role for Dmca1D in the processing of synaptic information in Drosophila motoneurons aCC and RP-2.