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      The Mechanistic Classification of Addictive Drugs

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      Author(s): * ,
      Publication date (Electronic):
      Journal: PLoS Medicine
      Publisher: Public Library of Science

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          Abstract

          The authors review recent research on the molecular mechanisms of addiction and propose a new classification for addictive drugs.

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          Most cited references55

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          Is there a common molecular pathway for addiction?

          Eric J. Nestler (2005)
          Drugs of abuse have very different acute mechanisms of action but converge on the brain's reward pathways by producing a series of common functional effects after both acute and chronic administration. Some similar actions occur for natural rewards as well. Researchers are making progress in understanding the molecular and cellular basis of these common effects. A major goal for future research is to determine whether such common underpinnings of addiction can be exploited for the development of more effective treatments for a wide range of addictive disorders.
          Article 0 comments Cited 260 times – based on 0 reviews     Review now
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            Opioids excite dopamine neurons by hyperpolarization of local interneurons.

            SW Johnson, RA North (1992)
            Increased activity of dopamine-containing neurons in the ventral tegmental area is necessary for the reinforcing effects of opioids and other abused drugs. Intracellular recordings from these cells in slices of rat brain in vitro showed that opioids do not affect the principal (dopamine-containing) neurons but hyperpolarize secondary (GABA-containing) interneurons. Experiments with agonists and antagonists selective for opioid receptor subtypes indicated that the hyperpolarization of secondary cells involved the mu-receptor. Most principal cells showed spontaneous bicuculline-sensitive synaptic potentials when the extracellular potassium concentration was increased from 2.5 to 6.5 or 10.5 mM; these were prevented by TTX and assumed to result from action potentials arising in slightly depolarized local interneurons. The frequency of these synaptic potentials, but not their amplitudes, was reduced by opioids selective for mu-receptors. It is concluded that hyperpolarization of the interneurons by opioids reduces the spontaneous GABA-mediated synaptic input to the dopamine cells. In vivo, this would lead to excitation of the dopamine cells by disinhibition, which would be expected to contribute to the positive reinforcement seen with mu-receptor agonists such as morphine and heroin.
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              Subsecond dopamine release promotes cocaine seeking.

              Paul Phillips, Garret Stuber, Michael Heien … (2003)
              The dopamine-containing projection from the ventral tegmental area of the midbrain to the nucleus accumbens is critically involved in mediating the reinforcing properties of cocaine. Although neurons in this area respond to rewards on a subsecond timescale, neurochemical studies have only addressed the role of dopamine in drug addiction by examining changes in the tonic (minute-to-minute) levels of extracellular dopamine. To investigate the role of phasic (subsecond) dopamine signalling, we measured dopamine every 100 ms in the nucleus accumbens using electrochemical technology. Rapid changes in extracellular dopamine concentration were observed at key aspects of drug-taking behaviour in rats. Before lever presses for cocaine, there was an increase in dopamine that coincided with the initiation of drug-seeking behaviours. Notably, these behaviours could be reproduced by electrically evoking dopamine release on this timescale. After lever presses, there were further increases in dopamine concentration at the concurrent presentation of cocaine-related cues. These cues alone also elicited similar, rapid dopamine signalling, but only in animals where they had previously been paired to cocaine delivery. These findings reveal an unprecedented role for dopamine in the regulation of drug taking in real time.
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                Author and article information

                Journal
                Journal ID (nlm-ta): PLoS Med
                Journal ID (publisher-id): pmed
                Title: PLoS Medicine
                Publisher: Public Library of Science (San Francisco, USA )
                ISSN (Print): 1549-1277
                ISSN (Electronic): 1549-1676
                Publication date (Print): November 2006
                Publication date (Electronic): 14 November 2006
                Volume: 3
                Issue: 11
                Electronic Location Identifier: e437
                Author notes
                * To whom correspondence should be addressed. E-mail: christian.luscher@ 123456medecine.unige.ch
                Article
                Publisher ID: 06-PLME-RIT-0259R1-APPEAL
                DOI: 10.1371/journal.pmed.0030437
                PMC ID: 1635740
                PubMed ID: 17105338
                SO-VID: 9a857cfa-c94e-4ea2-a2ae-92dbd9da1d2e
                Copyright © Copyright: © 2006 Lüscher and Ungless. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
                History
                Page count
                Pages: 6
                Categories
                Subject: Research in Translation
                Subject: Other
                Subject: Pharmacology/Drug Discovery
                Subject: Psychology
                Subject: Clinical Pharmacology
                Subject: Psychiatry
                Subject: Substance Use (Including Alcohol)
                Subject: Psychiatry
                Subject: Drug Misuse (Including Addiction)
                Subject: Drugs and Adverse Drug Reactions
                Custom metadata
                citation Lüscher C, Ungless MA (2006) The mechanistic classification of addictive drugs. PLoS Med 3(11): e437. doi: 10.1371/journal.pmed.0030437

                ScienceOpen disciplines: Medicine
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                ScienceOpen disciplines: Medicine

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