西亚试剂：Mice Genetically Deficient in Vasopressin V1a and V1b Recep

发布时间：2025-05-16

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

Yoshiaki Yamaguchi1,*, Toru Suzuki1,*, Yasutaka Mizoro1, Hiroshi Kori2,3, Kazuki Okada1, Yulin Chen1, Jean-Michel Fustin1, Fumiyoshi Yamazaki1, Naoki Mizuguchi1, Jing Zhang4, Xin Dong4, Gozoh Tsujimoto5, Yasushi Okuno6, Masao Doi1, Hitoshi Okamura1,4,†

Jet-lag symptoms arise from temporal misalignment between the internal circadian clock and external solar time. We found that circadian rhythms of behavior (locomotor activity), clock gene expression, and body temperature immediately reentrained to phase-shifted light-dark cycles in mice lacking vasopressin receptors V1a and V1b (V1a–/–V1b–/–). Nevertheless, the behavior of V1a–/–V1b–/– mice was still coupled to the internal clock, which oscillated normally under standard conditions. Experiments with suprachiasmatic nucleus (SCN) slices in culture suggested that interneuronal communication mediated by V1a and V1b confers on the SCN an intrinsic resistance to external perturbation. Pharmacological blockade of V1a and V1b in the SCN of wild-type mice resulted in accelerated recovery from jet lag, which highlights the potential of vasopressin signaling as a therapeutic target for management of circadian rhythm misalignment, such as jet lag and shift work.

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