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• W1492311868 abstract "In this issue of Addiction, Castells and his colleagues have surveyed and analyzed the literature on controlled clinical trials of central nervous system (CNS) stimulant medications for the treatment of cocaine dependence [1]. Five medications were analyzed in the meta-analysis; a slight but significant reduction in cocaine use was noted. The most promising of the medications analyzed are dexamphetamine and modafinil, although the evidence of efficacy for these two medications could rightly be considered preliminary. Further research is needed to substantiate the efficacy of these two medications. The development of medications for the treatment of cocaine dependence has been a top priority for the US National Institute on Drug Abuse (NIDA), National Institutes of Health. NIDA has used two strategic approaches, in this regard a ‘top-down’ and a ‘bottom-up’. The ‘top-down’ approach, featuring evaluation of the effect of marketed CNS pharmaceuticals on the use of cocaine, has been reviewed [2]. More than 60 marketed medications have been tested by NIDA-funded investigators, either alone or in combination. Several medications have shown promise to reduce cocaine use and are in confirmatory testing, modafinil among them. NIDA is funding three additional clinical trials evaluating the efficacy of modafinil to reduce cocaine use. Two of these are single-site trials and the third is a multi-site trial, currently being analyzed. When these additional trials are completed, they will be analyzed separately and then all three trials will be aggregated for a meta-analysis. It is anticipated that the results will confirm or refute the ability of modafinil to reduce cocaine use. Retention is also being assessed and will be analyzed. These trials address the recommendation of Dr Castells and his colleagues for additional testing on modafinil. Similarly, NIDA is also funding trials with d-amphetamine for the treatment of cocaine dependence. A clinical pharmacology study is evaluating the effects of d-amphetamine pre-treatment on the subjective effects of cocaine. One out-patient trial is exploring whether the combination of buprenorphine and sustained-release amphetamine will reduce opiate and cocaine use in dually dependent users, while another will evaluate the effects of amphetamine in combination with modafinil versus modafinil alone on cocaine use during treatment. Although published beyond the time-frame of the Castells group search, Levin and co-workers recently reported methylphenidate reduced cocaine use in a comorbid attention deficit hyperactive disorder (ADHD)/cocaine-dependent population, even though it did not alleviate the ADHD symptomatology to a greater extent than placebo [4]. These findings add to the database and suggest that further study of methylphenidate in cocaine dependence is also warranted. Studies in human cocaine users have shown that chronic cocaine use has profound and complex effects on the dopamine system. Volkow and colleagues have reported that cocaine users have reduced D2 dopamine receptors [5] and a decreased release of dopamine, compared to normal controls, when challenged with intravenous methylphenidate [6]. Post-mortem studies have noted that D3 dopamine receptors and D3 mRNA are increased in cocaine overdose victims [3,7]. A large (∼50%) increase in dopamine transporter density has been reported with concomitant reductions in caudate dopamine levels and the density of the striatal vesicular monoamine transporter [7]. How does this dysregulation of the dopamine system affect the treatment response? Two of the most desired outcomes of treating an individual with cocaine dependence are to help them to cease drug use and to value non-drug-related stimuli and rewards greater than drugs and drug-related stimuli. The thesis will be advanced that a major deficit exists in the valence of non-drug-related rewarding stimuli in dopamine deficiency states. Leyton and colleagues evaluated the effect of d-amphetamine on subjective responses and incentive salience in normal volunteers under normal conditions and acute depletion of dopamine (by administration of a diet deficient in tyrosine/phenylalanine). Although the subjective effects of d-amphetamine were not altered by the dopamine-deficient state, responses on a go/no go task were disrupted, especially when subjects were rewarded for making correct choices [8]. Administration of l-dopa reversed the effects of the dopamine dietary deficiency on the subjects' responses, suggesting that dopamine is necessary for the perception of salient cues and the ability to respond to them appropriately. Grabowski and colleagues [9] conducted two randomized clinical trials of levodopa–carbidopa versus placebo in cocaine-dependent subjects given cognitive behavioral therapy that failed to show an effect of apparently replenishing dopamine on cocaine use or retention. However, a third study of the levodopa–carbidopa combination showed a differential treatment effect favoring the drug combination when a reward contingency was added to the behavioral therapy (Schmitz, personal communication). Anticipation of monetary reward has been shown to activate the nucleus accumbens [10,11]. This suggests that apparent replenishment of dopamine can amplify the response to a non-drug-related reward state, one of the stated goals of therapy. Can replacement therapy work in the treatment of cocaine dependence? Studies being performed currently and those anticipated in the near future will go a long way to answering the question. And what are we replacing anyway with CNS stimulants? At the neurochemical level, I would say dopamine. At the neural circuit level, we may be replacing a constricted, dysregulated reward system with one that responds to rewards other than cocaine. My hypothesis is that the magnitude of the pharmacotherapy treatment response may be contingent upon dynamic activation of the reward system via a non-drug reinforcer." @default.
• W1492311868 created "2016-06-24" @default.
• W1492311868 date "2007-12-01" @default.
• W1492311868 modified "2023-09-23" @default.
• W1492311868 title "[Commentary] CAN REPLACEMENT THERAPY WORK IN THE TREATMENT OF COCAINE DEPENDENCE? AND WHAT ARE WE REPLACING ANYWAY?" @default.
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• W1492311868 doi "https://doi.org/10.1111/j.1360-0443.2007.02014.x" @default.
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