G(o )contributes to olfactory reception in Drosophila melanogaster

BACKGROUND: Seven-transmembrane receptors typically mediate olfactory signal transduction by coupling to G-proteins. Although insect odorant receptors have seven transmembrane domains like G-protein coupled receptors, they have an inverted membrane topology and function as ligand-gated cation channels. Consequently, the involvement of cyclic nucleotides and G proteins in insect odor reception is controversial. Since the heterotrimeric G(o)α subunit is expressed in Drosophila olfactory receptor neurons, we reasoned that G(o )acts together with insect odorant receptor cation channels to mediate odor-induced physiological responses. RESULTS: To test whether G(o )dependent signaling is involved in mediating olfactory responses in Drosophila, we analyzed electroantennogram and single-sensillum recording from flies that conditionally express pertussis toxin, a specific inhibitor of G(o )in Drosophila. Pertussis toxin expression in olfactory receptor neurons reversibly reduced the amplitude and hastened the termination of electroantennogram responses induced by ethyl acetate. The frequency of odor-induced spike firing from individual sensory neurons was also reduced by pertussis toxin. These results demonstrate that G(o )signaling is involved in increasing sensitivity of olfactory physiology in Drosophila. The effect of pertussis toxin was independent of odorant identity and intensity, indicating a generalized involvement of G(o )in olfactory reception. CONCLUSION: These results demonstrate that G(o )is required for maximal physiological responses to multiple odorants in Drosophila, and suggest that OR channel function and G-protein signaling are required for optimal physiological responses to odors.