How might signaling through ALK regulate behavioral responses to ethanol? In flies and mammalian cells in culture, ALK is known to activate the MAPK/ERK pathway [27], [34], [35], [36], [37], [38], [39]. We previously demonstrated that increased ERK signaling, through the receptor tyrosine kinase EGFR, in Drosophila neurons results in resistance to ethanol-induced sedation [5]. If ALK similarly stimulates ERK phosphorylation, then one would predict that loss of dAlk function would lead to decreased ERK phosphorylation and increased sensitivity to ethanol-induced sedation. However, the results described here indicate that reducing ALK levels instead leads to increased resistance to the sedating effect of ethanol in Drosophila. In an attempt to discern whether ERK phosphorylation is altered with loss of ALK function, we examined ERK phosphorylation in the heads of mutant f01491 flies by western blotting. We did not observe any changes in ERK under these conditions (AWL, CLK and UH, unpublished results). It is possible that levels of phosphorylated ERK are altered in a subset of neurons in the brain that we could not detect with western blotting of whole heads,
