Featured Review Cell Science Reviews Vol 5 No 3 ISSN 1742-8130

Calmodulin-dependent kinases in cocaine addiction

Cocaine addicts compulsively seek and consume cocaine. Even after long periods of withdrawal, a drug associated cue can trigger relapse. Recent evidence suggests that potentiated glutamatergic transmission in the brain reward circuitry may underpin cocaine craving and relapse. While it is known that cocaine rapidly and transiently elevates dopamine, it is not clear how repeated elevations in dopamine lead to adaptations in the reward circuitry that result in addiction. Calmodulin-dependent kinases (CaMKs) are known to mediate several aspects of glutamatergic synaptic plasticity. Here we review the most recent studies on the nucleus accumbens that suggest CaMKs may be involved in the process of addiction. We have not repeated many recent efforts to exhaustively review the role of CaMKs in glutamatergic synaptic plasticity, nor the role of synaptic plasticity in cocaine addiction. Rather, we briefly review normal DA function at the molecular, cellular and circuit levels. We then discuss recent data suggesting that CaMKs may mediate cocaine induced aberrations in glutamatergic transmission in the nucleus accumbens.

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