Limited involvement of Ca2+/calmodulin-dependent kinase II alpha and beta in mammalian sleep

While sleep is important, our understanding of its molecular mechanisms is limited. Over the last two decades, protein kinases have been implicated in sleep regulation, with a prominent role for Ca++/calmodulin-dependent kinase II (CaMKII) {beta}. Of all the known mouse genetic mutants, the biggest changes in sleep was reported to be observed in Camk2b gene knockout mice: sleep was reduced by approximately 120 minutes (mins) over 24 hours (hrs). We have reexamined the sleep phenotype in Camk2a and Camk2b knockout mice, and while we have observed sleep reduction in Camk2a knockout mice, we did not find sleep reduction in Camk2b mutants.We did find both Camk2a and Camk2b participated in homeostatic sleep rebound, though. Because CamKII and {beta} are widely known to be crucial kinases with interesting properties, it is worthwhile to keep our results in record for a general service to the field.