2002 East Coast Worm Meeting abstract 73
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
| 1 | Centre for Addiction and Mental Health,University of Toronto |
| 2 | University of California, San Diego |
| 3 | Universite de Montreal & Institute de Cardiologie de Montreal |
| 4 | Samuel Lunenfeld Research Institute, Mnt. Sinai Hospital, Toronto, Canada,University of Toronto |
Various dopamine-modulated behaviors, including motor response, reward and information processing, are subject to sensitization and habituation. Mal-adaptation of these processes are thought to play a role in learning and memory processes as related to addictions and psychosis. The underlying mechanisms of these processes are still poorly understood, and genetic approaches with C. elegans may allow the study of these mechanisms for dopamine mediated responses. A large body of evidence suggests that dopamine functions as a neurotransmitter in C. elegans modulating various behaviors, including egg laying, food sensing, and motility. Here we report the identification and functional characterization of a C. elegans dopamine receptor. The dar-1 gene encodes two alternatively spliced forms of the receptor recognizing catecholamines, with dopamine displaying the highest potency. Other amines did not activate the receptor. The absence of (nor)epinephrine in C. elegans indicates that dopamine is the likely endogenous ligand for this receptor. Functional coupling of the receptor was dependent on Gas. The dar-1 gene displays a restricted neural expression pattern including several neurons in the nerve ring and mechanosensory neurons like ALM and PLM. A deletion mutant for dar-1 (dar-1(ev748)) displayed altered behavioral responses to mechanosensory stimuli, but not previously established dopamine-related behaviors. The dar-1 mutant showed a greatly enhanced facilitation of accelerations in response to tap habituation training. This phenotype was rescued by a dar-1 wild-type transgene indicating that the DAR-1 receptor is required for modulation of mechanosensory behavioral plasticity.