ethanol-induced olfactory startle response (PS for Berlin: 5.9 ± 0.46 mm/s, Or83b1: 5.1 ± 0.90 mm/s, p = 0.471, paired t-test, n = 6), suggesting that ethanol odor is detected by Or83b-independent means, presumably by the 30% of OR neurons that retain functionality (Fig. 5A). Or83b mutant flies showed 2 specific alterations in ethanol-induced behaviors, reduced Dist during the first ethanol exposure, and an increased ΔDist (Fig. 5B,C). Neither behavioral change in Or83b mutants could be attributed to altered ethanol sedation sensitivity, and there was also no effect of the mutation on ethanol sedation tolerance (Fig. 5D,E). These data suggest that an Or83b-mediated olfactory mechanism promotes acute locomotor responding to ethanol, and that this mechanism is independent of the olfactory-mediated startle response. Down-regulation of Or83b gene expression following acute ethanol exposure may therefore contribute to increased locomotor activity that accompanies the development of rapid tolerance.
