Fiche publication
Date publication
janvier 2014
Auteurs
Membres identifiés du Cancéropôle Est :
Pr HAIECH Jacques
Tous les auteurs :
Bachstetter AD, Webster SJ, Tu T, Goulding DS, Haiech J, Watterson DM, Van Eldik LJ
Lien Pubmed
Résumé
The calcium/calmodulin-dependent protein kinase II (CaMKII) is abundant in the brain, where it makes important contributions to synaptic organization and homeostasis, including playing an essential role in synaptic plasticity and memory. Four genes encode isoforms of CaMKII (alpha, beta, delta, gamma), with CaMKIIalpha and CaMKIIbeta highly expressed in the brain. Decades of molecular and cellular research, as well as the use of a large number of CaMKIIalpha mutant mouse lines, have provided insight into the pivotal roles of CaMKIIalpha in brain plasticity and cognition. However, less is known about the CaMKIIbeta isoform. We report the development and extensive behavioral and phenotypic characterization of a CaMKIIbeta knockout (KO) mouse. The CaMKIIbeta KO mouse was found to be smaller at weaning, with an altered body mass composition. The CaMKIIbeta KO mouse showed ataxia, impaired forelimb grip strength, and deficits in the rotorod, balance beam and running wheel tasks. Interestingly, the CaMKIIbeta KO mouse exhibited reduced anxiety in the elevated plus maze and open field tests. The CaMKIIbeta KO mouse also showed cognitive impairment in the novel object recognition task. Our results provide a comprehensive behavioral characterization of mice deficient in the beta isoform of CaMKII. The neurologic phenotypes and the construction of the genotype suggest the utility of this KO mouse strain for future studies of CaMKIIbeta in brain structure, function and development.
Référence
PLoS One. 2014 Aug 15;9(8):e105191
