Activation of organum vasculosum neurones and water intake in mice by vasopressin neurones in the suprachiasmatic nucleus

Previous studies have shown that mice housed under a 12:12h light/dark cycle display a pronounced increase in water intake during a 2-h anticipatory period (AP) near the end of their active period (Zeitgeber Time ZT; ZT21.5-23.5) compared to the preceding basal period (BP, ZT19.5-21.5). This increased water intake during the AP is not associated with physiological stimuli for thirst, such as food intake, hyperosmolality, hyperthermia or hypovolaemia. Denying mice the water intake supplement during the AP causes them to be dehydrated at wake time. These observations suggest that this form of thirst may be driven by the circadian clock and serve to mitigate the dehydrating effect of an absence of water intake during sleep. Here, we review recent findings showing that this behaviour is mediated by vasopressin (VP) containing neurons in the suprachiasmatic nucleus (SCN). SCN VP neurones project to the organum vasculosum lamina terminalis (OVLT) where the activity dependent release of VP causes excitation of thirst-promoting neurones. SCN VP neurones increase their electrical activity during the AP and the resultant release of VP causes an increase in the action potential firing rate of OVLT neurones. Experiments involving optogenetic control of VP release from the axon terminals of SCN neurones indicate that this network mechanism is necessary and sufficient to mediate pre-sleep water intake in mice. These findings provide insight into the output mechanisms that are used by the central clock to generate circadian rhythms and also reveal that the regulation of water intake contributes to osmoregulatory homeostasis during sleep.