Insulin signaling in dopaminergic neurons regulates extended memory formation in Caenorhabditis elegans

Abstract

AbstractInsulin alters several brain functions, and perturbations in insulin levels could be a precipitating factor for Parkinson's disease, a disease associated with the degeneration of dopaminergic neurons. It is unclear whether insulin alters the dopamine signaling pathway and modulates learning and memory. In Caenorhabditis elegans, daf‐2 insulin receptor mutants have extended memory when trained for olfactory adaptation. In this study, we show that the absence of daf‐2 receptors in dopamine neurons results in this unusual learning behavior. Our results show that insulin function in memory is dopamine‐dependent. In the absence of the daf‐2 receptor, the calcium influx in dopamine neurons shows an altered pattern resulting in memory recall for an extended period. These results indicate that learning and memory involve insulin–dopamine crosstalk. Imbalances in this pathway result in changes in memory recall.