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Abstract
Loss of vasoactive intestinal polypeptide (VIP) or its receptor VPAC(2) disrupted circadian rhythms in approximately half of all SCN neurons.
- Vip(-/-) and Vipr2(-/-) mice exhibited two daily activity bouts in a skeleton photoperiod and multiple circadian periods in constant darkness.
- The absence of VIP or VPAC(2) abolished circadian firing rhythms in about 50% of SCN neurons.
- Disruption of synchrony was observed between rhythmic neurons lacking VIP or VPAC(2).
- Daily application of a VPAC(2) agonist restored rhythmicity and synchrony in VIP(-/-) SCN neurons, but not in Vipr2(-/-) neurons.
- VIP may coordinate daily rhythms in the SCN by synchronizing a small group of pacemaking neurons while maintaining rhythmicity in a larger subset.
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