Addiction is a reward deficit and stress surfeit disorder.
TLDR
The loss of reward function and recruitment of brain systems provide a powerful neurochemical basis that drives the compulsivity of addiction.Abstract:
Drug addiction can be defined by a three-stage cycle—binge/intoxication, withdrawal/negative affect, and preoccupation/anticipation—that involves allostatic changes in the brain reward and stress systems. Two primary sources of reinforcement, positive and negative reinforcement, have been hypothesized to play a role in this allostatic process. The negative emotional state that drives negative reinforcement is hypothesized to derive from dysregulation of key neurochemical elements involved in the brain reward and stress systems. Specific neurochemical elements in these structures include not only decreases in reward system function (within-system opponent processes) but also recruitment of the brain stress systems mediated by corticotropin-releasing factor (CRF) and dynorphin-κ opioid systems in the ventral striatum, extended amygdala, and frontal cortex (both between-system opponent processes). CRF antagonists block anxiety-like responses associated with withdrawal, block increases in reward thresholds produced by withdrawal from drugs of abuse, and block compulsive-like drug taking during extended access. Excessive drug taking also engages the activation of CRF in the medial prefrontal cortex, paralleled by deficits in executive function that may facilitate the transition to compulsive-like responding. Neuropeptide Y, a powerful anti-stress neurotransmitter, has a profile of action on compulsive-like responding for ethanol similar to a CRF1 antagonist. Blockade of the κ opioid system can also block dysphoric-like effects associated with withdrawal from drugs of abuse and block the development of compulsive-like responding during extended access to drugs of abuse, suggesting another powerful brain stress system that contributes to compulsive drug seeking. The loss of reward function and recruitment of brain systems provide a powerful neurochemical basis that drives the compulsivity of addiction.read more
Citations
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The Self-medication Hypothesis of Substance Use Disorders: A Reconsideration and Recent Applications
TL;DR: The self-medication hypothesis of addictive disorders derives primarily from clinical observations of patients with substance use disorders as mentioned in this paper, who discover that the specific actions or effects of each class of drugs relieve or change a range of painful affect states.
Journal ArticleDOI
Altering the course of schizophrenia: progress and perspectives
Millan Mark,Annie Andrieux,George Bartzokis,Kristin S. Cadenhead,Paola Dazzan,Paolo Fusar-Poli,Jürgen Gallinat,Jay N. Giedd,Dennis R. Grayson,Markus Heinrichs,René S. Kahn,Marie-Odile Krebs,Marion Leboyer,David A. Lewis,Oscar Marín,Philippe Marin,Andreas Meyer-Lindenberg,Patrick D. McGorry,Philip McGuire,Michael John Owen,Paul Patterson,Akira Sawa,Michael Spedding,Peter J. Uhlhaas,Flora M. Vaccarino,Claes Wahlestedt,Daniel R. Weinberger +26 more
TL;DR: A broad-based consideration of the challenges and opportunities inherent in efforts to alter the course of schizophrenia is provided, including 'hybrid' strategies that both relieve presenting symptoms and reduce the risk of transition to schizophrenia or another psychiatric disorder.
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The role of serotonin in drug use and addiction.
TL;DR: A new trajectory by which serotonergic neuroadaptations induced by first drug exposure pave the way for the establishment of addiction is suggested.
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Electrochemical Analysis of Neurotransmitters
TL;DR: A basic overview of the principles underlying constant-potential amperometry and fast-scan cyclic voltammetry, the most commonly employed electrochemical techniques, and the general application of these methods to the study of neurotransmission are provided.
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Heterogeneity of alcohol use disorder: Understanding mechanisms to advance personalized treatment.
TL;DR: Not surprisingly, given its heterogeneity, a wide variety of clinically acceptable treatment outcomes are possible with AUD, including not only abstinence, but also low-risk drinking (and even some less-conservative forms of moderate drinking).
References
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TL;DR: S sensitization of incentive salience can produce addictive behavior even if the expectation of drug pleasure or the aversive properties of withdrawal are diminished and even in the face of strong disincentives, including the loss of reputation, job, home and family.
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Positive reinforcement produced by electrical stimulation of septal area and other regions of rat brain.
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Drug addiction, dysregulation of reward, and allostasis.
George F. Koob,Michel Le Moal +1 more
TL;DR: The view that addiction is the pathology that results from an allostatic mechanism using the circuits established for natural rewards provides a realistic approach to identifying the neurobiological factors that produce vulnerability to addiction and relapse.