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

Abstract

Insulin 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.