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Dopamine in the Brain: Hypothesizing Surfeit or Deficit Links to Reward and Addiction
Kenneth Blum1, Peter K Thanos2, Marlene Oscar-Berman3
1Department of Psychiatry and McKnight Brain Institute, University of Florida, College of Medicine, Gainesville, FL, USA; Division of Nutrigenomics, La Vita RDS, Salt Lake City, UT, USA.
Brain dopamine plays a complex role in addiction. While acute drug use may involve dopamine "surfeit," chronic addiction and relapse are linked to dopamine "deficit" and dysregulation.
Area of Science:
- Neuroscience
- Addiction Research
- Neurobiology of Reward
Background:
- The role of brain dopamine (DA) in reward and addiction is debated, with theories ranging from DA's centrality in stimulant dependence to its lesser role in other addictions.
- Existing models propose "surfeit" (excess) or
- deficit
- (deficiency) theories to explain acute and chronic effects on brain reward circuitry.
- Understanding the nuances of dopamine's involvement requires distinguishing between hedonic impact ("liking"), reward prediction ("learning"), and incentive salience ("wanting").
Purpose of the Study:
- To review and synthesize competing explanatory frameworks for dopamine's role in reward and addiction.
- To clarify the distinctions between acute "surfeit" and chronic "deficit" models of dopamine function in addiction.
- To propose dopamine homeostasis as a therapeutic target for combating addiction relapse.
Main Methods:
- Literature review of studies investigating dopamine's role in acute and chronic reward circuitry responsivity.
- Analysis of evidence supporting "liking," "learning," and "wanting" models of dopamine function.
- Examination of findings related to dopamine signaling changes during chronic drug self-administration and non-substance-related addictive behaviors.
Main Results:
- Acute drug effects and Reward Deficiency Syndrome (RDS) behaviors are often associated with dopamine "surfeit" and hyperdopaminergic states.
- Chronic excessive substance use, such as cocaine, is linked to decreased phasic dopamine signaling in the striatum.
- Addiction progression shows blunted responsivity at brain reward sites, and relapse may be associated with dopamine deficiency.
Conclusions:
- The "dopamine hypothesis" of addiction is complex, involving hedonic tone, attention, reward expectancy, and incentive motivation.
- Dopamine homeostasis is disrupted in chronic addiction, with relapse potentially driven by dopamine deficiency.
- Genetic predispositions, neurotransmitter interactions, and stress contribute to addiction vulnerability and relapse, underscoring the importance of restoring dopamine balance.
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