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Neuroreport. 2002 Jun 12;13(8):1013-6.

CaMKII regulates amphetamine-induced ERK1/2 phosphorylation in striatal neurons.

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  • 1Division of Pharmacology, School of Pharmacy, University of Missouri-Kansas City, 2411 Holmes St., M3-C15, Kansas City, MO 64108, USA.


Amphetamine activates extracellular signal-regulated kinase 1 and 2 (ERK1/2) resulting in cAMP response element-binding protein (CREB) and Elk-1 phosphorylation in striatal neurons. In the present study we investigated whether calcium and calmodulin-dependent protein kinase II (CaMKII) regulates amphetamine-induced ERK1/2 pathways in striatal neurons using Western blot and immunohistochemical analysis. Acute administration of amphetamine (5 mg/kg, i.p.) increased phosphorylated (p)CaMKII immunoreactivity. Inhibition of CaMKII by intrastriatal infusion of KN62 (2, 10, or 25 nmol) attenuated amphetamine-induced increases in pERK1/2, pCREB, and pElk-1 immunoreactivity in the ipsilateral dorsal striatum in a dose-dependent manner. These data suggest that CaMKII controls amphetamine-activated ERK1/2 pathways in striatal neurons in vivo.

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