[28]. We hypothesized that this may be one mechanism by which worms develop AFT to ethanol. If AFT requires modulation of SLO-1 function, then complete loss of SLO-1 should reduce or eliminate the development of tolerance. In an otherwise wild-type background, null slo-1(eg142) mutant animals are quite resistant to the sedative effects of ethanol on locomotion, and, importantly, do not develop significant tolerance to ethanol (Figure 4b). We asked if loss of slo-1 completely eliminated the ability of animals to develop tolerance, even in a genetic background of fast development of tolerance. In the sensitized npr-1(ky13) mutant background, slo-1(eg142) animals, that lack SLO-1, are able to develop a degree of tolerance (Figure 4b), indicating that modulation of the ethanol effect on SLO-1 occurs during AFT but that SLO-1 is not the sole mediator of AFT.
