Journal
SCIENCE
Volume 342, Issue 6154, Pages 85-90Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1238599
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Funding
- Ministry of Education, Science, Sports and Culture of Japan
- Takeda Science Foundation
- SRF
- Kanae Science Foundation
- Grants-in-Aid for Scientific Research [23590107, 24111526] Funding Source: KAKEN
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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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