title: Dopamine modulation of avoidance behavior in Caenorhabditis elegans requires the NMDA receptor NMR-1.
abstract: The nematode C. elegans utilizes a relatively simple neural circuit to mediate avoidance responses to noxious stimuli such as the volatile odorant octanol. This avoidance behavior is modulated by dopamine. cat-2 mutant animals that are deficient in dopamine biosynthesis have an increased response latency to octanol compared to wild type animals, and this defect can be fully restored with the application of exogenous dopamine. Because this avoidance behavior is mediated by glutamatergic signaling between sensory neurons and premotor interneurons, we investigated the genetic interactions between dopaminergic signaling and ionotropic glutamate receptors. cat-2 mutant animals lacking either the GLR-1 or GLR-2 AMPA/kainate receptors displayed an increased response latency to octanol, which could be restored via exogenous dopamine. However, whereas cat-2 mutant animals lacking the NMR-1 NMDA receptor had increased response latency to octanol they were insensitive to exogenous dopamine. Mutants that lacked both AMPA/kainate and NMDA receptors were also insensitive to exogenous dopamine. Our results indicate that dopamine modulation of octanol avoidance requires NMR-1, consistent with NMR-1 as a potential downstream signaling target for dopamine.
authors.affiliation: Department of Biology, California State University San Bernardino, San Bernardino, CA, United States of America.
authors.forename: Melvin
authors.initials: M
authors.lastname: Baidya
authors.affiliation: Department of Biology, California State University San Bernardino, San Bernardino, CA, United States of America.
authors.forename: Marx
authors.initials: M
authors.lastname: Genovez
authors.affiliation: Department of Biology, California State University San Bernardino, San Bernardino, CA, United States of America.
authors.forename: Marissa
authors.initials: M
authors.lastname: Torres
authors.affiliation: Department of Biology, California State University San Bernardino, San Bernardino, CA, United States of America.
authors.forename: Michael Y
authors.initials: MY
authors.lastname: Chao
mesh_terms: D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects*; D001522:Behavior, Animal / Q000187:drug effects*; D017173:Caenorhabditis elegans / Q000187:drug effects / Q000502:physiology*; D029742:Caenorhabditis elegans Proteins / Q000378:metabolism*; D004298:Dopamine / Q000494:pharmacology*; D004843:Epistasis, Genetic / Q000187:drug effects; D018698:Glutamic Acid / Q000378:metabolism; D009043:Motor Activity / Q000187:drug effects; D009154:Mutation / Q000235:genetics; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D000442:Octanols / Q000494:pharmacology; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D029742:Caenorhabditis elegans Proteins; C436186:NMR-1 protein, C elegans; D000442:Octanols; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid; D004298:Dopamine
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