Many organisms rely on the process of neuronal autophagy to maintain proper neurological function, with decreased neuronal autophagic function being correlated with human diseases such as Parkinson’s, Alzheimer's, and Huntington's diseases. By the use of signaling molecules, cells are able to both positively and negatively regulate autophagy. Di-homo-γ-linoleic acid (DGLA) is one such signaling molecule, and has been shown to positively regulate autophagy. The Lipid Binding Protein, lbp-3, serves as a lipid chaperone in C. elegans, shuttling DGLA from intestinal fat deposits to neurons. Because of what is known of both DGLA’s effect on autophagy and the effect of decreased autophagy on neurological health, it was hypothesized that RNAi knockdown of lbp-3 (lbp-3i) would induce a decline in neurological function in the affected nematodes. To test the hypothesis, thrashing assays were conducted to examine differences in mobility between control and lbp-3i nematodes both under normal and stressed (heat stress) conditions. Additionally, a chemotaxis assay was conducted to observe differences in learning and memory, exposing both control and lbp-3i nematodes to compounds present in prior heat-stressed conditions and monitoring their responses. While further investigation must be done to explore the relationship between the other LBPs and neurological function, it appears that lbp-3 plays an important role in regulating neuronal autophagy.