The catecholamine dopamine (DA) is a catecholamine neurotransmitter found in both vertebrates and invertebrates, where it modulates a wide variety of behaviors including movement, attention and reward. In humans, disruption of DA levels and signaling are associated with multiple brain disorders, including Parkinson’s disease, Schizophrenia, Attention Hyperactivity Disorder (ADHD) and addiction. In the nematode C. elegans, DA supports motor and sensory function, with excess DA transmission triggering Swimming-Induced Paralysis (Swip), a readily visible phenotype that we have shown to be well-suited to forward genetic efforts to identify DA regulatory genes. Here we describe our efforts to characterize two mutant lines, vt39 and vt44, isolated in an EMS-based screen for animals exhibiting Swip. Similar to DA transporter (dat-1) mutants, the Swip exhibited by vt39 and vt44 is rescued by either treatment of animals with the vesicular monoamine transporter (cat-1) inhibitor reserpine or by crossing these lines to animals that lack expression of the D2-type DA receptor DOP-3. Direct genomic sequencing, and complementation tests, indicate that both lines harbor a normal dat-1 gene. Using a single nucleotide polymorphism-based mapping approach, we find that vt39 and vt44 map to chromosomes I and III, respectively. Fine mapping and whole genome sequencing are underway to identify the genes mutated in these lines, efforts to be followed by genomic and cDNA rescue efforts to validate gene identification and to determine cell autonomy with respect to Swip induction. Supported by NIH Award MH095044 (R.D.B.) and MH093102 (J.A.H.).