| First Author | Andersen JM | Year | 2020 |
| Journal | Behav Brain Res | Volume | 390 |
| Pages | 112676 | PubMed ID | 32407818 |
| Mgi Jnum | J:291830 | Mgi Id | MGI:6443734 |
| Doi | 10.1016/j.bbr.2020.112676 | Citation | Andersen JM, et al. (2020) CaMKII is activated in opioid induced conditioned place preference, but alphaCaMKII Thr286 autophosphorylation is not necessary for its establishment. Behav Brain Res 390:112676 |
| abstractText | Activation of calcium/calmodulin-dependent protein kinase II (CaMKII), particularly its alpha isoform, is known to be important for neuronal processes central for learning and memory and has also been implicated in the maladaptive learning involved in drug addiction.Thr286 autophosphorylation of alphaCaMKII has been shown to be indispensable for establishment of cocaine-induced CPP (Easton et al., 2014). To study the contribution of CaMKII in opioid induced conditioned learning, we examined how establishment of conditioned place preference (CPP) induced by 10 or 30 mumol/kg morphine or its active metabolite morphine-6-glucuronide (M6G) affects the levels and Thr286 autophosphorylation of the alpha- and beta-isoforms of CaMKII, as well as beta-actin levels, in dorsal and ventral striatum and in hippocampus of mice. An acute and a sub-chronic treatment were used as controls. Whereas an acute single administration of morphine or M6G caused increases in CaMKII levels and phosphorylation at Thr286 and beta-actin in striatal areas, CPP induced by these opioids was accompanied primarily by an increase in the protein levels of both CaMKII isoforms and beta-actin in dorsal striatum and hippocampus. Decreases in CaMKII Thr286 phosphorylation were observed in dorsal striatum after the sub-chronic pharmacological treatment. Despite the changes observed in alphaCaMKII activity in wild type mice, morphine-induced CPP was not affected in alphaCaMKII(T286A) autophosphorylation-deficient mice. These results indicate that opioid-induced CPP is accompanied by activation of alpha- and betaCaMKII in striatum and hippocampus, but, in opposition to what has been observed with cocaine, alphaCaMKII autophosphorylation is not essential for establishment of opioid-induced CPP. |
