were able to respond normally to external stimuli as evidenced by the normal magnitude ethanol olfactory startle response in naive animals (mean PS Berlin: 6.1 ± 0.49 mm/s, AcCoASf03474: 6.2 ± 0.49 mm/s, p = 0.823, paired t-test, n = 6). Upon second exposure, AcCoASf03474 showed a markedly reduced startle response (mean PS Berlin: 5.4 ± 0.54 mm/s, AcCoASf03474: 2.3 ± 0.16 mm/s, p = 0.003, paired t-test, n = 6) and a delayed onset of hyperactivity, but showed a normal increase in ΔDist during the descending phase of the hyperactivity response (Fig. 4E). Additionally, AcCoASf03474 flies showed normal ethanol sedation tolerance (Fig. 4G). These data suggest that biochemical pathways that depend on acetyl-CoA production via AcCoAS contribute to ethanol-induced hyper-activity in naive animals.
