Clinical researchers have tried to identify drugs to reduce cocaine craving and prevent relapse. Numerous drugs looked promising in initial open-label trials but did not prove efficacious in subsequent placebo-controlled studies. These pharmacological treatments have included dopaminergic agonists (e.g., monamine oxidase inhibitors, amantadine, mazindol, methylphenidate, pemoline, bromocriptine, L-dopa, and pergolide), neurotransmitter precursors (L-tyrosine, L-tryptophan, and multivitamins with B complex), carbamazepine, and antide-pressants, including desipramine and fluoxetine. In a meta-analysis examining 45 clinical trials examining mostly antidepressants, carbamazepine, and dopa-mine agonists, no significant impact of drug treatment was found, regardless of the type of drug or dose used (Lima, Soares, Reisser, & Farrell, 2002).
Clinical trials with bupropion, olanzapine, naltrexone, buprenorphine, and other drugs are ongoing. As our understanding of the neurobiological basis of cocaine addiction becomes further refined, new pharmacological strategies are emerging. Potential targets include specific dopamine, serotonin, and other receptor subtypes, neuroendocrine peptides (i.e., CRF), and biogenic amine transporters, including the dopamine reuptake transporter. These pharmaco-therapies and the potential development of a vaccine to prevent cocaine from reaching its CNS site of action are covered in Chapter 26.
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