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.
Highlights
A basic function of the nervous system is to confer the ability to detect external stimuli and to generate appropriate behavioral and physiological responses
We have found that the avoidance behavior to octanol in C. elegans is modulated by the biogenic monoamine dopamine
While the AMPA/kainate ionotropic glutamate receptor subunits GLR-1 and GLR-2 are required for normal octanol response, exogenous dopamine improved response latency
Summary
A basic function of the nervous system is to confer the ability to detect external stimuli and to generate appropriate behavioral and physiological responses. These responses can be modulated when parallel streams of information are provided to the nervous system and neural activity is appropriately altered. A classic example of this is the effect of addictive narcotics such as cocaine via a dopaminergic pathway on glutamatergic synapses in the ventral tegmental area [1] Another example is the modulation of silent synapses in nociceptive interneurons in the spinal cord via descending serotonergic output from the rostroventromedial medulla [2]. We report that C. elegans avoidance response to the noxious stimulant 1-octanol is modulated by dopamine
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