Translating the neuroscience of alcoholism into clinical treatments: From blocking the buzz to curing the blues

Heilig, Markus; Thorsell, Annika; Sommer, Wolfgang H.; Hansson, Anita C.; Ramchandani, Vijay A.; George, David T.; Hommer, Daniel; Barr, Christina S.

doi:10.1016/j.neubiorev.2009.11.018

Cited by 117Neurotransmitter Receptor Influence on BehaviorSubstance Abuse Treatment and OutcomesNeuroscience and Neuropharmacology Research

Translating the neuroscience of alcoholism into clinical treatments: From blocking the buzz to curing the blues

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Heilig, Markus, Thorsell, Annika, Sommer, Wolfgang H., Hansson, Anita C., Ramchandani, Vijay A., George, David T., Hommer, Daniel, Barr, Christina S.·2010·Neuroscience & Biobehavioral Reviews

DOI 10.1016/j.neubiorev.2009.11.018PMC PMC2891917

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Abstract

Understanding the pathophysiology of addictive disorders is critical for development of new treatments. A major focus of addiction research has for a long time been on systems that mediate acute positively reinforcing effects of addictive drugs, most prominently the mesolimbic dopaminergic (DA) system and its connections. This research line has been successful in shedding light on the physiology of both natural and drug reward, but has not led to therapeutic breakthroughs. The role of classical reward systems is perhaps least clear in alcohol addiction. Here, recent work is summarized that points to some clinically important conclusions. First, important pharmacogenetic differences exist with regard to positively reinforcing effects of alcohol and the ability of this drug to activate classical reward pathways. This offers an opportunity for personalized treatment approaches in alcoholism. Second, brain stress and fear systems become pathologically activated in later stages of alcoholism and their activation is a major influence in escalation of alcohol intake, sensitization of stress responses, and susceptibility to relapse. These findings offer a new category of treatment mechanisms. Corticotropin-releasing hormone (CRH) signaling through CRH1 receptors is a major candidate target in this category, but recent data indicate that antagonists for substance P (SP) neurokinin 1 (NK1) receptors may have a similar potential.

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Chronic drug use is characterized by compulsive drug-taking behavior despite negative consequences.
“Although initial drug intake is associated with positive reinforcement and impulsive actions, chronic drug use is characterized by compulsive drug-taking behavior despite negative consequences.4, 5, 6”
From Behavioral and neuroimaging evidence for overreliance on habit learning in alcohol-dependent patients (2013) · cites this paper as [5]
To date, treatment programs for AD have mainly tried to reduce the positive reinforcing properties of drugs or to reduce the negative reinforcing aspects of chronic alcohol use represented by relief craving.
“To date, treatment programs for AD have mainly tried to reduce the positive reinforcing properties of drugs (‘blocking the buzz' for example, with the opioid antagonist naltrexone) or to reduce the negative reinforcing aspects of chronic alcohol use represented by relief craving (‘curing the blues' for example, with acamprosate).5”
From Behavioral and neuroimaging evidence for overreliance on habit learning in alcohol-dependent patients (2013) · cites this paper as [5]

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Substantial attributable risk related to a functional mu-opioid receptor gene polymorphism in association with heroin addiction in central Sweden
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REVIEW: Genetically selected Marchigian Sardinian alcohol‐preferring (msP) rats: an animal model to study the neurobiology of alcoholism
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Accentuated Decrease in Social Interaction in Rats Subjected to Repeated Ethanol Withdrawals
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IMAGING STUDY: Modulation of brain response to emotional images by alcohol cues in alcohol‐dependent patients
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Neurokinin-1 Receptor-Expressing Neurons in the Amygdala Modulate Morphine Reward and Anxiety Behaviors in the Mouse
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A mu-opioid receptor single nucleotide polymorphism in rhesus monkey: association with stress response and aggression
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Substance P in Stress and Anxiety
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Association of a Functional Polymorphism in the μ-Opioid Receptor Gene With Alcohol Response and Consumption in Male Rhesus Macaques
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“Using this model, we found increased psychomotor stimulation in response to alcohol, increased alcohol preference, and increased frequency of alcohol consumption at a level leading to intoxication in carriers of the rhesus (rh) OPRM1 77G variant (Barr et al., 2007).”
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Lack of self-administration and behavioural sensitisation to morphine, but not cocaine, in mice lacking NK1 receptors
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A temporal threshold for induction of persistent alcohol preference: behavioral evidence in a rat model of intermittent intoxication.
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CLINICAL PREDICTORS OF RESPONSE TO NALTREXONE IN ALCOHOLIC PATIENTS: WHO BENEFITS MOST FROM TREATMENT WITH NALTREXONE?
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Heterogeneous effects of alcohol on dopamine release in the striatum: a PET study.
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PRECLINICAL STUDY: Region‐specific down‐regulation of Crhr1 gene expression in alcohol‐preferring msP rats following ad lib access to alcohol
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Can experimental paradigms and animal models be used to discover clinically effective medications for alcoholism?
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OPRM1 Asn40Asp Predicts Response to Naltrexone Treatment: A Haplotype‐Based Approach
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Getting closer to affective disorders: the role of CRH receptor systems
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The NK1-receptor antagonist NKP608 has an antidepressant-like effect in the chronic mild stress model of depression in rats
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Functional CRH variation increases stress-induced alcohol consumption in primates
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Low doses of methylnaloxonium in the nucleus accumbens antagonize hyperactivity induced by heroin in the rat
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Repeated Cycles of Chronic Intermittent Ethanol Exposure Leads to the Development of Tolerance to Aversive Effects of Ethanol in C 57 BL /6 J Mice
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On the role of ascending dopamine systems in the control of voluntary ethanol intake and ethanol intoxication
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Development of an Alcohol Deprivation and Escalation Effect in C57BL/6J Mice
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Suppression of Alcohol Preference by Naltrexone in the Rhesus Macaque: A Critical Role of Genetic Variation at the μ-Opioid Receptor Gene Locus
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Inhibition of shock-induced foot tapping behaviour in the gerbil by a tachykinin NK1 receptor antagonist
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Neurokinin 1 Receptor Antagonism Promotes Active Stress Coping Via Enhanced Septal 5-HT Transmission
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Increased anxiety and other similarities in temperament of alcoholics with and without antisocial personality disorder across three diverse populations
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Stress-induced release of substance P in the locus coeruleus modulates cortical noradrenaline release
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Place aversion induced by the substance P analogue, dimethyl-C7, is not state dependent: implication of substance P in aversion
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Mood and neuroendocrine response to a chemical stressor, metyrapone, in buprenorphine-maintained heroin dependence
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Pharmacogenetic studies of alcohol self-administration and withdrawal
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Neurocircuitry for modeling drug effects
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P.6.a.008 Personality disorders in patients with alcohol abuse and alcoholism: an exploratory study
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Recent Developments in Decoding Neurobiological Pathways and Treatment Targets in Alcohol Dependence
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Authors: Heilig, M., Thorsell, A., Sommer, W. H., Hansson, A. C., Ramchandani, V. A., George, D. T., Hommer, D., & Barr, C. S.
Affiliations: National Institutes of Health (US)
Corresponding author: Heilig, Markus
ORCID: Heilig, Markus
Thorsell, Annika
Sommer, Wolfgang H.
Hansson, Anita C.
Ramchandani, Vijay A.
George, David T.
Barr, Christina S.
Venue: Neuroscience & Biobehavioral Reviews
Publisher: Elsevier BV
Published: 2010-11
Volume: 35
Issue: 2
Pages: 334-344
ISSN: 0149-7634 (ISSN-L)
DOI: 10.1016/j.neubiorev.2009.11.018
PMC: PMC2891917
OpenAlex: W2010733076
Cited by: 117
References: 144
Citations by year: 2026: 2 · 2025: 3 · 2024: 1 · 2023: 4 · 2022: 3 · 2021: 5 · 2020: 2 · 2019: 5 · 2018: 3 · 2017: 11 · 2016: 9 · 2015: 11 · 2014: 13 · 2013: 9 · 2012: 15
FWCI: 4.99
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neuroscience & Biobehavioral Reviews (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
National Institute on Alcohol Abuse and Alcoholism (ZIAAA000487)
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 › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords: alcoholism, mesolimbic dopamine system, drug reward, pharmacogenetics, personalized treatment, relapse, corticotropin-releasing factor, substance P, NK1 receptor antagonists
MeSH terms: CRF Receptor, Type 1, Ethanol, Alcoholism, Animals, Brain, Corticotropin-Releasing Hormone, Humans, Models, Biological, Substance P, Drug Delivery Systems, Receptors, Corticotropin-Releasing Hormone, Translational Research, Biomedical, Neurokinin-1 Receptor Antagonists

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Translating the neuroscience of alcoholism into clinical treatments: From blocking the buzz to curing the blues

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