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Calcium-Calmodulin-Dependent Protein Kinase Type 2
Inhibition of CaMKII in the nucleus accumbens shell decreases enhanced amphetamine intake in sensitized rats.
Transient overexpression of alpha-Ca2+/calmodulin-dependent protein kinase II in the nucleus accumbens shell enhances behavioral responding to amphetamine.
Transient viral-mediated overexpression of alpha-calcium/calmodulin-dependent protein kinase II in the nucleus accumbens shell leads to long-lasting functional upregulation of alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptors: dopamine type-1 receptor and protein kinase A dependence.
Persistent reversal of enhanced amphetamine intake by transient CaMKII inhibition.