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Titlebook: Drug Addiction; From Basic Research Rao S. Rapaka,Wolfgang Sadée Book 2008 Springer-Verlag New York 2008 Addiction.Basic.Cannabinoid.Chemo

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https://doi.org/10.1007/978-3-662-10798-0, DA can influence CART in the accumbens. Thus a complex interacting circuitry likely exists. Fifth, in humans, CART is altered in the ventral tegmental area of cocaine overdose victims, and a mutation in the CART gene associates with alcoholism..Overall, it is clear that there are functional intera
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https://doi.org/10.1007/978-3-662-10798-0XCL10/IP 10, CCL3/MIP-1α, and CCL5/RANTES. Functional roles for the chemokine system, composed of the chemokine ligands and their receptors, have been suggested in brain development and heterologous desensitization. The system can alter the actions of neuronally active pharmacological agents such as
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https://doi.org/10.1007/978-3-662-10798-0he expression of peripheral nAChRs in cells other than neurons and how they participate in fundamental processes, such as inflammation. Understanding these processes may offer novel therapeutic strategies to approach inflammatory diseases, as well as precautions in the design of interventional drugs
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https://doi.org/10.1007/978-3-662-10798-0tivity and subcellular distribution of monoamine transporters, a phenomenon likely related to the neurotoxic potential of these drugs to DAergic neurons. This article will review some of the recent findings whereby releasers and uptake blockers alter DAT and VMAT-2 activity and how these alterations
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https://doi.org/10.1007/978-3-662-10798-0pounds substitute for cocaine, reduce the intake of cocaine in rats and rhesus monkeys trained to self-administer cocaine, and have demonstrated a slow onset and long duration of action and lack of sensitization. The 3-phenyltropane analogs were also tested in a rhesus monkey self-administration mod
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https://doi.org/10.1007/978-3-662-10798-0gh affinity molecular targets for drugs of abuse including cocaine, amphetamine, and 3,4-methylenedioxymetamphetamine (MDMA) “Ecstasy.” Monoamine transporters also serve as molecular gateways for neurotoxins. Emerging evidence indicates that regulation of transporter function and surface expression
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