The suprachiasmatic nucleus (SCN) in the brain is dubbed the master clock of internal circadian rhythms, and using a histochemistry-based screening strategy the authors first showed that expression levels of AVP as well as the V1A and V1B receptors were particularly high in this brain region. Next, they went on to examine the behaviour and expression patterns of selected circadian clock genes in the SCN of mice deficient in both of these receptors (Avpr1a−/−Avpr1b−/− mice) under normal and jet-lag-simulated conditions. For 2 weeks, wild-type mice and Avpr1a−/−Avpr1b−/− mice were housed in conditions of 12-hour light and 12-hour dark cycles. After this, jet lag was simulated by advancing the light–dark cycle by 8 hours.
Before jet lag was induced, both types of mice were equally active during the dark phase, indicating that the absence of the V1A and V1B receptors in mice did not lead to overt differences in behaviour. In addition, expression of the canonical circadian clock genes (Per1, Per2, Bma1 and Dbp) in the SCN was similar between wild-type and Avpr1a−/−Avpr1b−/− mice. After jet lag was induced, it took wild-type mice 8–10 days to synchronize the time when they became active to the actual time when the dark phase began (that is, to re-entrain). In Avpr1a−/−Avpr1b−/− mice, re-entrainment took 2–4 days. Moreover, in wild-type mice, expression of Per1, Per2, Bma1 and Dbp took 8–9 days to return to the original circadian rhythm of expression, whereas it took 3 days in Avpr1a−/−Avpr1b−/− mice.
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