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

• DOI: 10.1126/science.1238599
• Publication Date: 2013-10-03T18:15:45Z
• Authors: Yoshiaki Yamaguchi; Toru Suzuki; Yasutaka Mizoro; Hiroshi Kori; Kazuki Okada; Yulin Chen; Jean-Michel Fustin; Fumiyoshi Yamazaki; Naoki Mizuguchi; Jing Zhang; Xin Dong; Gozoh Tsujimoto; Yasushi Okuno; Masao Doi; Hitoshi Okamura
• Keywords: Jet Lag Syndrome; Mice, Knockout; 0301 basic medicine; Receptors, Vasopressin; CLOCK Proteins; Cell Communication; Motor Activity; Body Temperature; Circadian Rhythm; Mice; 03 medical and health sciences; Gene Expression Regulation; Animals; Suprachiasmatic Nucleus; Antidiuretic Hormone Receptor Antagonists; Cells, Cultured

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.