CONTRIBUTIONS OF EAG PROTEIN TO NEURONAL EXCITABILITY IN IDENTIFIED THORACIC MOTONEURONS OF DROSOPHILA by

Diversity in the expression of ion channel proteins among neurons allows a wide range of excitability, growth and functional regulation. Ether-a-go-go (EAG), a member of the voltage-gated K channels, was characterized by spontaneous firing in nerve terminals and enhanced neurotransmitter release. In situ whole-cell patch-clamp recordings performed from the somata of Drosophila larval thoracic aCC motoneurons revealed spontaneous spike-like events in eag mutants. Spontaneous events were absent in wild type motoneurons. Spikes evoked by somatic current injection in to the cell body were not altered and comparable to wild type. Spontaneous spike-like events could be due to increased synaptic drive or altered intrinsic excitability of the motoneuron. Reduction of EAG function with selective expression of eag double stranded RNAi transgene in motoneurons only did not cause spontaneous spike-like events or alter evoked firing. This suggests increased synaptic drive contributes to spontaneous events. Both transient and sustained voltage-activated K currents, each with Casensitive (IA(Ca) and IK(Ca)) and Ca -insensitive components (IA and IK), were isolated in thoracic aCC motoneurons. In wild type motoneurons, IA was larger than IA(Ca). Conversely, IK(Ca) was larger than IK. Both eag mutants and eag RNAi expression resulted in a decrease in IA , IK and a slow sustained K current. Further, EAG and Shal demonstrate a potential functional interaction and contribute to IA. The voltage sensitivity for inactivation was reduced in Shal only and EAG-Shal double knock down compared to