Answers are grounded in this paper and cite their sources.
Animal study uncovers that CaMKIIα mediates wheel-running feedback to the master circadian pacemaker in mice, indicating a key molecular mechanism linking physical activity to biological clocks.
CaMKIIα functional knockout mouse (K42R) showed substantial changes in the entrainment pattern of running-wheel (RW) rhythm to a short (LD6:18) but not to a long (LD18:6) photoperiod. In wild type mice (WT), entrainment to LD6:18 occurred at the light-off phase, whereas in most K42R entrainment took place at the light-on phase. These differences are well explained by lengthening of circadian period (τ) and compromising the couplings between the activity-onset and -end in K42R. Indeed, τ in K42R and WT were longer and shorter than 24 h, respectively, under the following constant darkness (DD). Without RW τ was lengthened in WT, whereas it was shortened in K42R. Similarly, activity time was lengthened in WT but shortened in K42R. Importantly, τ without RW was not different between the two genotypes, which were confirmed in naive mice. Tau and α returned to the pre-removal levels after RW re-introduction in both WT and K42R. These results indicate that the changes of behavioral rhythm in K42R are due to a lack of feedback effects of RW activity, which are mediated by CaMKIIα-dependent mechanisms. A two-oscillator model assuming involvement of CaMKIIα in the coupling between them successfully simulated the effects of RW activity in K42R.
No takes yet. Share an insight, caveat, or question.
Yoshikawa et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: