Mice Genetically Deficient in Vasopressin V1a and V1b Receptors Are Resistant to Jet Lag

Abstract

Resetting the Circadian Clock Fatigue and other symptoms of jet lag arise when the body's internal circadian clock is out of sync with environmental light-dark cycles. Studying genetically modified mice lacking two receptors for the peptide hormone vasopressin under experimental conditions simulating jet lag, Yamaguchi et al. (p. 85 ; see the Perspective by Hastings ) concluded that vasopressin signaling in the suprachiasmatic nucleus (SCN)—a region of the brain known to control circadian rhythms—impedes adjustment to the environmental clock. Infusion of vasopressin receptor antagonists directly into the SCN of wild-type mice accelerated their recovery from jet lag, suggesting that this pathway may merit further investigation as a pharmacological target for treating jet lag.