There is cross-talk between CaMKII, ERK, and PKA pathways, with CaMKII modulating stimulant-induced activation of ERK and PKA. In vitro, CaMKII inhibitors attenuate acute nicotine-induced ERK phosphorylation in mouse striatal neurons.37 In rat striatal neurons, acute treatment with a dopamine D1 receptor agonist75 and an NMDA agonist240 increases levels of p-CREB, which is attenuated by the CaMKII inhibitor KN62. In vivo in rats, intrastriatal infusion of the CaMKII inhibitor KN62 dose-dependently inhibits increases in p-ERK and p-CREB induced by acute administration of amphetamine.236
