Abstract
Oxygen is vital for neuron development and function, and low oxygen (hypoxia) or 0% oxygen available (anoxia) conditions lead to neuronal dysfunction and death. Nonlethal forms of stress, prior to hypoxic or anoxic (preconditioning) environments protects neurons and increases survival to oxygen deprivation. Hyperpolarization of C. elegans neurons prior to anoxia (neural preconditioning) increases survival, but the cellular and molecular pathways that confer survival are unclear. Here we report that loss in ceramide synthase gene, hyl-2 suppresses increased survival to anoxia in neural preconditioned animals, suggesting that HYL-2 functions upstream of the circuit that regulates neural preconditioning.