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Dopamine receptor signaling in a model circuit

Drug abuse is a chronic and devastating disease, costing society over 200 billion per year. The problem is widespread; in 2004, over 34 million Americans reported lifetime use of cocaine. Persistent use of cocaine leads to maladaptations in reward-related learning such that the drug is prized above all other rewards, and is compulsively sought after and used, despite severe negative consequences (addiction). Cocaine elevates the concentration of the neurotransmitter, dopamine (DA), at the synapse. It is not clear how repeated, prolonged elevations in [DA] disrupt the normal mechanisms of associative learning and memory. Such processes depend, in part, upon the flow of ions through channels in the neuronal membrane (ion currents); and both cocaine and DA are known to alter ion current densities. The Baro lab uses a model circuit to elucidate the processes by which brief versus prolonged elevations in DA lead to changes in ion current densities. DA acts by binding to DA receptors, which in turn, activate signal transduction cascades that can alter levels of the second messenger, cAMP. In this latest paper from her dissertation research, Clark demonstrates that DA-induced changes in cAMP are determined both by the functional properties of the receptors and the cellular milieu. Comparative Biochemistry and Physiology, Part B 146 (2007) 9-19.

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