The neurotransmitter dopamine regulates chemosensory avoidance behavior in the model organism Caenorhabditis elegans. Avoidance behaviors are mediated by the polymodal ASH nociceptive sensory neurons, and behavioral avoidance of stimuli detected by ASH is less robust when dopamine signaling is impaired. Our broad research goals are to understand the underlying molecular and cellular mechanisms of how dopamine modulates the activity of neural circuits. Using a custom microfluidics device and the transgenically-expressed Ca2+ sensor GFP variant G-CaMP, we have begun to characterize the ASH neural response of wild type and dopamine-deficient cat-2 mutant C. elegans when treated with exogenous dopamine and stimulated with the osmolyte glycerol. Our preliminary data suggest that exogenous dopamine perfused into the recording buffer in the microfluidics device affects ASH neuron excitability in cat-2 mutants. Our ongoing efforts now focus on optimizing our assay conditions (including type of stimuli to use and recording buffer components) and identifying molecular elements in ASH neurons that mediate this response, including the relevant dopamine receptor(s).