Involvement of genes encoding a K+ channel (ether a go-go) and a Na+ channel (smellblind) in Drosophila olfaction.
We have investigated the roles of the putative cyclic nucleotide-modulated K+ channel subunit encoded by the ether a go-go (eag) gene and a voltage-gated Na+ channel, smellblind (sbl), encoded by the paralytic (para) locus in odorant responsiveness and cell excitability in Drosophila melanogaster. Three independent mutant alleles of eag revealed reduced antennal responsiveness in adult flies to a subset of odorants, all having short aliphatic side chains: ethyl butyrate (EB), propionic acid, 2-butanone and ethyl acetate (manuscript submitted). Loose patch recordings revealed that significantly fewer eag antennal neurons responded to EB compared to control neurons. As expected if Eag were involved in odor transduction, fewer EB-induced inhibitory responses were observed in eag mutants and focal application of high K+ saline to sensillae altered the excitability of the majority of neurons from wild-type, but not eag, antennae. Interestingly, there were fewer excitatory odorant responses dependent on extracellular Ca2+ in eag neurons. In contrast to the involvement of Eag in adult olfactory neuron odorant transduction, we found no evidence that adult sbl and allelic olfactory D (olfD) gene mutants were defective in their behavioral response to a complex attractive odor. Furthermore, electrophysiological analyses of adult sbl and olfD mutants revealed normal electroantennogram responses to a broad range of individual pure odorants and no changes in the excitable properties of olfactory neurons as determined by loose patch recordings.