The Journal of Neuroscience, August 1, 1998, 18(15):5603-5613
The K+ Channel Gene Ether a Go-Go Is
Required for the Transduction of a Subset of Odorants in Adult
Drosophila melanogaster
Adrienne E.
Dubin,
Margaret M.
Liles, and
Greg L.
Harris
Department of Biology and Molecular Biology Institute, San Diego
State University, San Diego, California 92182-4614
The functional identity of an olfactory receptor neuron is
determined in part by its repertoire of responses to odorants. As an
approach toward understanding the contributions of particular conductances to olfactory neuron excitability and odor discrimination, we have investigated the role of the putative cyclic
nucleotide-modulated K+ channel subunit encoded by
the ether a go-go (eag) gene in odorant responsiveness in Drosophila melanogaster. Four
independent mutant eag alleles exhibited reduced
antennal sensitivity to a subset of nine odorants, all having short
aliphatic side chains: ethyl butyrate (EB), propionic acid, 2-butanone,
and ethyl acetate. Significantly fewer eag antennal
neurons responded to EB compared with control neurons; the proportion
sensitive to 2-heptanone was similar to controls. Two aspects of the
character of EB-induced excitability were affected by mutations in
eag. First, fewer EB-induced inhibitory responses were
observed in eag mutants, and second, fewer excitatory
odorant responses dependent on extracellular Ca2+
were observed. Furthermore, modulation of neuronal excitability by
membrane-permeant cyclic nucleotide analogs was largely
eag dependent. Focal application of high
K+ saline to sensillae altered the excitability of
the majority of neurons from wild-type but not eag
antennae, suggesting that Eag may have a dendritic
localization.
Key words:
ether a go-go; eag; potassium channel; Drosophila; electroantennogram; specific; Ca2+; cyclic nucleotide analogs; mutant; olfaction
Copyright © 1998 Society for Neuroscience 0270-6474/98/18155603-11$05.00/0