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Aramendy M.,University of Fribourg | Seibert S.,AG Functional Cell Biology | Treppmann P.,AG Functional Cell Biology | Richter K.,AG Functional Cell Biology | And 2 more authors.
Journal of Circadian Rhythms | Year: 2013

Background: Mammals can adapt to changing light/dark conditions by advancing or delaying their circadian clock phase. Light pulses evoke changes in gene expression and neuronal activity in the suprachiasmatic nuclei (SCN), the central pacemaker of the circadian system. Alterations in neuronal activity are partially mediated by changes in synaptic vesicle (SV) fusion at the presynaptic membrane, which modulates release of neurotransmitters.Methods: Male synaptophysin (Syp) knock-out and littermate control wild type mice were tested in an Aschoff type I resetting paradigm. Additionally, gene expression of cFos, Per1 and Per2 was assessed in the SCN. Finally, complexes between the synaptic vesicle proteins Syp and synaptobrevin (Syb) were studied in order to correlate behavior with protein complexes at synaptic vesicles.Results: Here we show that mice lacking Syp, a modulator of neurotransmitter release, are defective in delaying clock phase. In contrast, clock phase advances as well as clock period are normal in Syp -/- knock-out mice. This correlates with the formation of Syp/Syb complexes.Conclusions: Our findings suggest that Syp is involved specifically in the response to a nocturnal light pulse occurring in the early night. It appears that the SV component Syp is critically involved in the delay portion of the resetting mechanism of the circadian clock. © 2013 Aramendy et al.; licensee BioMed Central Ltd.

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