CaMKII regulates amphetamine-induced ERK1/2 phosphorylation in striatal neurons
- 1 June 2002
- journal article
- research article
- Published by Wolters Kluwer Health in NeuroReport
- Vol. 13 (8) , 1013-1016
- https://doi.org/10.1097/00001756-200206120-00006
Abstract
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.Keywords
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