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. 2017 Dec 6;37(49):11894–11911. doi: 10.1523/JNEUROSCI.2397-17.2017

Figure 3.

Figure 3.

Pharmacological inhibition of CaMKIIα/β in the dorsal hippocampus induces a deficit in extinction of cocaine CPP. A, Total and phosphorylated CaMKIIα, as well as phosphorylated CaMKIIβ, in the PSD-enriched fraction from the hippocampus were significantly higher after extinction of cocaine CPP compared with saline control mice. Total CaMKIIβ trended higher but did not reach statistical significance. B, Total and phosphorylated CaMKIIα in the PSD-enriched fraction from the hippocampus were significantly lower in mice that acquired cocaine CPP followed by home cage exposure without extinction training compared with saline control mice. Phosphorylated CaMKIIβ trended lower but did not reach statistical significance. *p < 0.05, **p < 0.01 compared with saline group. C, Timeline of surgery, CPP conditioning, acquisition test, and microinjection of the CaMKII α/β inhibitor KN93 or vehicle before extinction training. D, Similar acquisition of cocaine CPP was observed within each designated group before treatment during extinction training. ***p < 0.001 compared with baseline test. E, Infusion of KN93 into the dorsal hippocampus of mice (n = 7) before the each extinction training session attenuated extinction compared with vehicle-infused mice (n = 7). *p < 0.05 compared with vehicle group. Data are presented as mean ± SEM.