Abstract
The suprachiasmatic nucleus (SCN) circadian clock is critical for optimising daily cycles in mammalian physiology and behaviour. The roles of the various SCN cell types in communicating timing information to downstream physiological systems remain incompletely understood, however. In particular, while vasoactive intestinal polypeptide (VIP) signalling is essential for SCN function and whole animal circadian rhythmicity, the specific contributions of VIP cell output to physiological control remains uncertain. Here we reveal a key role for SCN VIP cells in central clock output. Using multielectrode recording and optogenetic manipulations, we show that VIP neurons provide coordinated daily waves of GABAergic input to target cells across the paraventricular hypothalamus and ventral thalamus, supressing their activity during the mid to late day. Using chemogenetic manipulation, we further demonstrate specific roles for this circuitry in the daily control of heart rate and corticosterone secretion, collectively establishing SCN VIP cells as influential regulators of physiological timing.
Highlights
The suprachiasmatic nucleus (SCN) circadian clock is critical for optimising daily cycles in mammalian physiology and behaviour
We evaluated the impact of brief (0.3–3 ms) blue light flashes via an optical fibre positioned over the SCN during perforated multielectrode array (pMEA)
This effect plateaued for ≥2 ms flashes, where the distribution of electrode sites showing optogenetic responses matched that expected for SCN vasoactive intestinal polypeptide (VIP) cells[30,31,32,34,35]
Summary
The suprachiasmatic nucleus (SCN) circadian clock is critical for optimising daily cycles in mammalian physiology and behaviour. The ability to adjust physiology and behaviour in anticipation of daily changes in the environment is critical for survival Mammals achieve this via a master circadian clock in the suprachiasmatic nucleus (SCN) whose role is to coordinate rhythms in cells and tissue function throughout the body according to predictable individual daily variations in demand[1,2,3]. While various studies have reported deficits in physiological/behavioural rhythms in mice lacking VIP or its receptor VPAC222–29, the loss of this signalling pathway produces a global disruption of SCN rhythmicity[18,19,20,21] These generalised impairments, obscure any specific roles for VIP cells in physiological control
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