Dataset for: NF-kappaB signalling is involved in immune-modulation, but not basal functioning, of the mouse suprachiasmatic circadian clock.

Circadian rhythms are recurring near-twenty four hour patterns driven by an endogenous circadian timekeeping system. The master pacemaker in this system is the hypothalamuc suprachiasmatic nucleus (SCN) . Recently interest has been drawn to how the SCN clock responds to immune system stimulation. A major signalling component in the immune system is nuclear factor (NF)-kappaB. In the present study we examined the role of NF-kappaB in SCN function. Whilst serum shocked fibroblasts showed rhythmic nuclear localisation of p65 and p65-dependent transcription, there were no circadian changes in the SCN in expression of the NF-kappaB components p65, c-Rel, p-IkappaB or p-IKK. Chronic treatment with the NF-kappaB inhibitor PDTC did not impact on circadian or diurnal rhythms. Phase-shifting light pulses did not impact on SCN expression of p65, and PDTC treatment did not attenuate the behavioural or molecular response to light pulses. Peripheral treatment with lipopolysaccharide resulted in increased NF-kappaB component expression in the SCN. In vitro experiments with SCN slice cultures showed that treatment with NF-kappaB inhibitors did not markedly alter rhythmic changes in PER2::LUC expression. Further, SCN slices from nf-kappab::luc mice did not show any evidence for circadian rhythms in NF-kappaB-mediated transcription. Experiments utilising older mice (~16 months old) showed that SCN treatment in vitro with PDTC resulted in increased amplitude of rhythmic PER2::LUC expression, and LPS treatment resulted in altered PER2::LUC rhythm acrophase. Overall, we interpret our results as providing evidence for the involvement of NF-kappaB in the suprachiasmatic circadian clock following immune stimulation, but not under basal conditions.