The molecular mechanisms that underlay learning and memory are still remained to be understood. The study of mechanisms of neural plasticity has been facilitated by simple conditioning paradigms such as habituation. We therefore undertook genetic analyses of the habituation behavior abnormal mutants:
hab-1(
cn308)LGI,
hab-2(
cn312)LGI,
hab-3(
cn350)LGIV,
hab-4(
cn303)LGV,
hab-5(
cn408)LGV,
hab-6(
cn358)LGIV,
hab-7(
cn352),
hab-9(
cn404) (WBG 12,116 1992). When compared to wild-type animals, these mutants were classified into three groups based on habituation pattern : more slowly habituated but more rapidly recovered from habituation
(cn308 and
cn350), more rapidly habituated but more slowly recovered (
cn312,
cn408,
cn358 and
cn352), and normally habituated but more rapidly recovered
(cn303). The associative learning behavior of the mutants were also tested. C. elegans is chemoattracted but repelled to NaCl under starved condition(Saeki et al.,J.Exp.Biol. 204 1757 2001). Under the assay condition,
cn308,
cn312,
cn350 and
cn303 showed abnormal behavior. That is, both
cn308 and
cn312 mutants showed no attraction and repellence:
cn350 partially attracted but
cn303 are weakly repelled. Testing of an another learning paradigm on chemotactic behavior toward diacetyl after training with repetitive exposure to diacetyl-acetic acid stimuli(Morrison et al.,Behavioral Neurosci. 113,358 1999) is also in progress. In addition to abnormal learning behaviors, the hab mutants show behavioral abnormalities. For example,
hab-2 mutants are defective in both the nose-touch response and the osmotic avoidance, suggesting that
hab-2 functions in the ASH sensory neurons. To elucidate its function, we are now cloning these genes by cosmid rescue experiments.