Similarly, mutations in eat-4, which codes for a vesicular glutamate transporter expressed in ASH and other glutamatergic neurons, result in a loss of response to sensory stimuli. Thus, the primary sensory transduction pathway is, at least in part, mediated by glutamatergic neurotransmission. ASH neurons have dense core Raddeanoside-R8 vesicles at their Yohimbine-Hydrochloride synapses and express many different neuropeptide genes. Neuropeptides encoded by nlp-3 likely play a role in the primary pathway for octanol response. In mammals, interactions between dopamine signaling and NMDA signaling have been well characterized. For instance, D1 type dopamine receptors can signal through classic second messenger pathways, including cAMP/PKA and phospholipase C/Ca2+/PKC, both of which lead to increases in NMDA responses. By contrast, D2-type dopamine receptors cause decreases in NMDA responses. Dopamine receptors can also physically interact with NMDA receptors to regulate their activity. For instance, in rat hippocampal neurons the C-terminal domain of the D1 dopamine receptor directly interacts with NMDA receptor subunits NR1-1a and NR2A. The first interaction directly inhibits NMDA currents, whereas the second interaction attenuates NMDA-mediated excitotoxicity via PI-3 kinase. In the striatum, D1 receptors co-immunoprecipitate with NR1 NMDA subunits, and D1/NR1 complexes may play a role in receptor trafficking. Herein, we characterize a novel genetic interaction between NMDA and dopamine signaling in C. elegans. We show that the C. elegans avoidance response to 100% octanol is modulated by dopamine. Wild type animals respond robustly to octanol, whereas cat-2 mutant animals, which are deficient for dopamine biosynthesis, respond with increased response latency. This defect is fully restored with exogenous dopamine. Whereas the AMPA/kainate receptor subunits GLR-1 and GLR-2 are dispensable for dopamine sensitivity, the NMDA receptor subunit NMR-1 is absolutely required. The dopamine receptors DOP-1, DOP-2, and DOP-3 are redundantly required for normal response.