New perspectives on cocaine addiction: recent findings from animal research
Abstract
Research with laboratory animals has provided several insights into the nature of cocaine abuse and addiction. First, the nature of drug addiction has been reevaluated and the emphasis has shifted from physical dependence to compulsive drug-taking behavior. Second, animal studies suggest that cocaine is at least as addictive as heroin and possibly even more addictive. Third, cocaine is potentially more dangerous than heroin as evidenced by the higher fatality rate seen in laboratory animals given unlimited access to these drugs. Fourth, the neural basis of cocaine reinforcement has been identified and involves an enhancement of dopaminergic neurotransmission in the ventral tegmental dopamine system. Other addictive drugs (e.g., opiates) may also derive at least part of their reinforcing impact by pharmacologically activating this reward system. Fifth, although the biological consequences of repeated cocaine self-administration on central nervous system functioning are poorly understood, preliminary findings suggest that intravenous cocaine self-administration may decrease neural functioning in this brain reward system. This has important clinical implications because diminished functioning of an important brain reward system may significantly contribute to relapse into cocaine addiction. These and other findings from experimentation with laboratory animals suggest new considerations for the etiology and treatment of drug addiction.Key words: addiction, cocaine, dopamine, reward, withdrawal syndrome.
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Substance-use disorders are typically accompanied by decreased reward motivation for typical and non-pathological rewards, termed motivational toxicity or reward-deficiency syndrome.
“As a number of researchers have described [106,149], substance-use disorders are typically accompanied by decreased reward motivation for typical and non-pathological rewards, a phenomenon that has been variously termed ‘motivational toxicity’ [150] and ‘reward-deficiency syndrome’ [151].”
From Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings (2012) · cites this paper as [150]
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- Authors
- Bozarth, M. A.
- Affiliations
- University at Buffalo, State University of New York (US)
- Corresponding author
- Bozarth, Michael A.
- Venue
- Canadian Journal of Physiology and Pharmacology
- Publisher
- Canadian Science Publishing
- Published
- 1989-09-01
- Volume
- 67
- Issue
- 9
- Pages
- 1158-1167
- ISSN
- 0008-4212 (ISSN-L)
- 1205-7541
- OpenAlex
- W2036471732
- Cited by
- 47
- References
- 43
- Citations by year
- 2026: 1 · 2023: 1 · 2013: 2 · 2012: 1
- FWCI
- 1.35
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Canadian Journal of Physiology and Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Epidemiology › Substance Abuse Treatment and Outcomes
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Keywords
- cocaine dependence, cocaine self-administration, ventral tegmental area, dopamine signaling, relapse, drug addiction treatment
- MeSH terms
- Animals, Cocaine, Substance-Related Disorders
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