Summer Research Description: Disruptions in the coordination of dopamine (DA) and glutamate (GLU) signaling have been linked to various brain disorders including schizophrenia, addiction, and Parkinson’s Disease. The signaling pathways that support DA and GLU signaling are highly conserved from worm to man, making C. elegans a useful model system for studying their interactions. Loss of function mutations in the C. elegans gene, swip-10, within glial cells leads to increased DA neuron excitability and a hyperdopaminergic phenotype that is rescued by loss of glutamate vesicular packaging or loss of glutamate receptors. swip-10 mutant animals also display morphological changes of their DA neurons reminiscent of the early stages of DA neuron degeneration seen after 6-hydroxydopamine exposure. We hypothesize that the increased levels of extracellular GLU driving DA hypersecretion also leads to changes in the morphology of swip-10 DA neurons. We aim to assess morphological changes by quantifying the incidence of missing soma, shrunken soma, and breaks in DA neurons in wild type and swip-10 mutants. Additionally, we aim to address whether these morphological changes are dependent on DA and/or GLU signaling. Understanding this glial-expressed glutamatergic regulator of DA signaling may reveal novel insights to the molecular underpinnings of neurodegenerative disorders such as Parkinson’s disease.