| First Author | Lavoie J | Year | 2013 |
| Journal | Behav Brain Res | Volume | 253 |
| Pages | 262-5 | PubMed ID | 23919927 |
| Mgi Jnum | J:202353 | Mgi Id | MGI:5518517 |
| Doi | 10.1016/j.bbr.2013.08.001 | Citation | Lavoie J, et al. (2013) Glycogen synthase kinase-3beta haploinsufficiency lengthens the circadian locomotor activity period in mice. Behav Brain Res 253:262-5 |
| abstractText | The mood stabiliser drug lithium has been reported to impact circadian rhythms in vertebrates. Among several putative therapeutic molecular targets, direct inhibition of glycogen synthase kinase-3 beta (GSK3beta) by lithium has been proposed to underlie its effects on circadian physiology. Here we study the effect of GSK3beta haploinsufficiency on the circadian locomotor activity in mice during a free-running period in comparison to wildtype littermates (WT). Mice were housed individually to record their circadian wheel running activity and were entrained to a 12h light/12h dark cycle for 14 days and then placed under constant darkness for 14 days to allow free-running. During the free-running phase, the circadian locomotor activity period of GSK3beta(+/-) was significantly lengthened (23.83+/-0.05h) when compared to the WT mice (23.54+/-0.10h; p=0.0374). No significant difference in locomotor activity was observed. Knowing that GSK3beta interacts with most of the core clock components, these data suggest that GSK3beta acts as a critical intrinsic regulator of the circadian clock and plays an important role in regulating its period in response to lithium treatment. |
