We are interested in olfactory adaptation, a component of behavioral plasticity. To investigate the gene(s) involved in olfactory adaptation, we screened for the mutants defective in adaptation to odorants. From out of 4,000 EMS-mutagenized animals, we isolated 11 mutants exhibiting defects in adaptation to the AWC-sensed odorants. One of the mutants turned out to contain a mutation in
gei-1, that encodes Rho-GAP (GTPase-activated protein). To investigate whether Rho-GTPase(s) acts in this behavior, we examined olfactory adaptation of transgenic animals expressing dominant active/negative forms of Rho-GTPase family. The dominant active RHO-1 inhibited normal olfactory adaptation as the
gei-1 mutant. Furthermore, the genetic analyses indicate that RHO-1 acts downstream of GEI-1 and UNC-13 acts downstream of RHO-1 in olfactory adaptation. Next, to investigate whether the neurotransmitter Acetylcholine is important for the olfactory adaptation, we examined the effect of levamisole (activating Acetylcholine receptor) on the olfactory adaptation of wild-type strain. We found that the levamisole-treatment perturbs normal olfactory adaptation.