Major Depressive Disorder (MDD) is the leading cause of disability worldwide. One of MDD's most troubling symptoms is the loss of reward firing, or anhedonia. Current publications indicate that MTCH‐2, a gene associated with mitochondrial transport, is related to a decrease in firing rates in the hippocampus of mice. Additionally, a GWAS reported a link between MTCH‐2 and neuroticism in humans. Consequently, we hypothesize that a MTCH‐2 related decrease in firing rates in the nucleus accumbens could potentially play a role in the development of depressive symptoms.The C. Elegans MTCH‐1 protein shows a 87% homology to the human MTCH‐2 protein. Here, we examine the relationship between the MTCH‐1 gene and C. Elegans reward firing. Because C. Elegans reward firing levels have been associated with changes in speed change fluidity in past studies, we measure C. Elegans motility as a proxy for reward firing. In this study, we compare motility and gene expression in MTCH‐1 deficient worms and wt worms and further examine MTCH‐1 knockdown to control motility. Together, these data points may indicate a role of MTCH‐2 in depression.Support or Funding InformationThe Nueva SchoolThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.