Acute administration of psychostimulants has variable effects on CaMKII activity depending on the particular stimulant drug and brain region examined. In rats, acute cocaine treatment (15 mg/kg i.p.) increases CaMKII activity in the NAc,235 whereas acute amphetamine treatment (5 mg/kg i.p.) increases CaMKII activity in the striatum236 and produces several downstream CaMKII-dependent events. Inhibition of CaMKII activity with KN93 attenuates acute amphetamine-induced dopamine efflux from mouse striatal neurons, brain slices, and, in vivo, from the dorsal striatum.237 In mouse striatal synaptosomes, acute amphetamine administration decreases dopamine transporter expression at the cell surface, and this effect is attenuated by KN93.238 In contrast to these effects of amphetamine, acute treatment with methamphetamine (5 mg/kg i.p.) decreases CaMKII activity in the rat striatum, parietal cortex, NAc, frontal cortex, and hippocampus.239
