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Article ; Online: Endogenous opioids and addiction to alcohol and other drugs of abuse.

Gianoulakis, Christina

2009 Volume 9, Issue 11, Page(s) 999–1015

Abstract: There is significant experimental evidence implicating the endogenous opioid system (opioid peptides and opioid receptors) with the processes of reward and reinforcement. Indeed, many behaviors associated with reward and reinforcement, for example ... ...

Abstract	There is significant experimental evidence implicating the endogenous opioid system (opioid peptides and opioid receptors) with the processes of reward and reinforcement. Indeed, many behaviors associated with reward and reinforcement, for example feeding behavior, are controlled by distinct components of the endogenous opioid system located in relevant brain regions. It has also been shown that regardless of their initial site of action many drugs of abuse, such as morphine, nicotine, cocaine, alcohol and amphetamines, induce an increase in the extracellular concentration of dopamine in the nucleus accumbens. This, increased secretion of dopamine in the nucleus accumbens seems to be a common effect of many drugs of abuse, and it was proposed that may mediate their rewarding and reinforcing properties. Furthermore, activation of mu opioid receptors in the ventral tegmental area, or of mu and delta opioid receptors in the nucleus accumbens enhances the extracellular concentration of dopamine in the nucleus accumbens. Thus, stimulation of the activity of distinct components of the endogenous opioid system either by opioid or by other drugs of abuse, may mediate some of their reinforcing effects. In this review article, a brief description of the endogenous opioid system and its implication in the processes of reward and reinforcement of opioid and other drugs of abuse will be presented. Furthermore, the use of opioid antagonists in the treatment of drug addiction will be discussed. Special emphasis will be given to ethanol addiction, the drug mainly studied in my laboratory.
MeSH term(s)	Alcoholism/physiopathology ; Brain/physiopathology ; Humans ; Motivation ; Opioid Peptides/physiology ; Substance-Related Disorders/physiopathology
Chemical Substances	Opioid Peptides
Language	English
Publishing date	2009-09-09
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2064823-6
ISSN	1873-4294 ; 1568-0266
ISSN (online)	1873-4294
ISSN	1568-0266
DOI	10.2174/156802609789630956
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Article: Alterations in brain levels of atrial and C-type natriuretic peptides after chronic moderate ethanol consumption in spontaneously hypertensive rats.

Guillaume, P / Gutkowska, J / Gianoulakis, C

European journal of pharmacology

1997 Volume 319, Issue 2-3, Page(s) 215–224

Abstract: Atrial (ANP) and C-type (CNP) natriuretic peptides have been found in brain regions associated ...

Abstract	Atrial (ANP) and C-type (CNP) natriuretic peptides have been found in brain regions associated with fluid homeostasis and blood pressure. Since chronic moderate ethanol consumption has been shown to prevent the age-dependent increase in blood pressure in experimental animals, the objective of the present studies was to investigate the effect of ethanol (20% (v/v) for 8 months) on the total content and concentration of ANP and CNP in the brain of spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. Ethanol increased the content and concentration of both ANP and CNP in the hypothalamus, pons and medulla of SHR rats. In contrast, in the WKY rats ethanol had no effect on the levels of ANP in any of the brain regions studies, but enhanced the concentration of CNP in the hypothalamus and medulla. Thus, ethanol induced changes in the content of natriuretic peptides in distinct brain regions associated with control of cardiovascular activity. Such changes may be partially responsible for the effect of chronic moderate ethanol consumption on blood pressure.
MeSH term(s)	Aging/metabolism ; Alcohol Drinking/metabolism ; Animals ; Blood Pressure/drug effects ; Brain Chemistry/drug effects ; Hypertension/genetics ; Hypertension/metabolism ; Hypothalamus/drug effects ; Hypothalamus/metabolism ; Iodine Radioisotopes ; Male ; Medulla Oblongata/drug effects ; Medulla Oblongata/metabolism ; Natriuretic Peptide, C-Type ; Pons/drug effects ; Pons/metabolism ; Proteins/metabolism ; Radioimmunoassay ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Species Specificity
Chemical Substances	Iodine Radioisotopes ; Proteins ; Natriuretic Peptide, C-Type (127869-51-6)
Language	English
Publishing date	1997-01-29
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/s0014-2999(96)00869-2
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Article: Alcohol-seeking behavior: the roles of the hypothalamic-pituitary-adrenal axis and the endogenous opioid system.

Gianoulakis, C

Alcohol health and research world

2005 Volume 22, Issue 3, Page(s) 202–210

Abstract: Both the hormones of the hypothalamic-pituitary-adrenal (HPA) axis and the endogenous opioid system are activated in response to stress as well as after alcohol consumption, supporting the hypothesis that stress can influence both alcohol consumption and ...

Abstract	Both the hormones of the hypothalamic-pituitary-adrenal (HPA) axis and the endogenous opioid system are activated in response to stress as well as after alcohol consumption, supporting the hypothesis that stress can influence both alcohol consumption and craving for alcohoL Activation of the HPA axis by stress or alcohol results in the production of glucocorticoid hormones, such as cortisol. Those hormones, in turn, are important for the release of the brain chemical dopamine in certain brain areas that are associated with the rewarding and reinforcing effects of alcohol and other drugs. Alcohol-induced release of certain endogenous opioids similarly results in dopamine release in those brain regions. Through this mechanism, both the HPA axis and the endogenous opioid system may influence alcohol consumption. Consequently, genetically determined differences in the activities of the HPA axis and endogenous opioid system may help determine a person's alcohol consumption level and vulnerability to alcoholism.
MeSH term(s)	Alcohol Drinking/genetics ; Alcohol Drinking/metabolism ; Alcohol Drinking/physiopathology ; Animals ; Behavior, Addictive/genetics ; Behavior, Addictive/metabolism ; Behavior, Addictive/physiopathology ; Humans ; Hypothalamo-Hypophyseal System/metabolism ; Hypothalamo-Hypophyseal System/physiology ; Hypothalamo-Hypophyseal System/physiopathology ; Opioid Peptides/physiology ; Pituitary-Adrenal System/metabolism ; Pituitary-Adrenal System/physiology ; Pituitary-Adrenal System/physiopathology
Chemical Substances	Opioid Peptides
Language	English
Publishing date	2005-02-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	427760-0
ISSN	0090-838X
ISSN	0090-838X
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Article: Endogenous opioids and addiction to alcohol and other drugs of abuse.

Gianoulakis, Christina

Current topics in medicinal chemistry

2003 Volume 4, Issue 1, Page(s) 39–50

Abstract	There is significant experimental evidence implicating the endogenous opioid system (opioid peptides and opioid receptors) with the processes of reward and reinforcement. Indeed, many behaviors associated with reward and reinforcement, for example feeding behavior, are controlled by distinct components of the endogenous opioid system located in relevant brain regions. It has also been shown that regardless of their initial site of action many drugs of abuse, such as morphine, nicotine, cocaine, alcohol and amphetamines, induce an increase in the extracellular concentration of dopamine in the nucleus accumbens. This increased secretion of dopamine in the nucleus accumbens seems to be a common effect of many drugs of abuse, and it was proposed that may mediate their rewarding and reinforcing properties. Furthermore, activation of micro opioid receptors in the ventral tegmental area, or of micro and delta opioid receptors in the nucleus accumbens enhances the extracellular concentration of dopamine in the nucleus accumbens. Thus, stimulation of the activity of distinct components of the endogenous opioid system either by opioid or by other drugs of abuse, may mediate some of their reinforcing effects. In this review article, a brief description of the endogenous opioid system and its implication in the processes of reward and reinforcement of opioid and other drugs of abuse will be presented. Furthermore, the use of opioid antagonists in the treatment of drug addiction will be discussed. Special emphasis will be given to ethanol addiction, the drug mainly studied in my laboratory.
MeSH term(s)	Alcoholism/drug therapy ; Alcoholism/metabolism ; Animals ; Brain/drug effects ; Brain/metabolism ; Dopamine/metabolism ; Endorphins/metabolism ; Ethanol/metabolism ; Humans ; Nucleus Accumbens/drug effects ; Nucleus Accumbens/metabolism ; Opioid Peptides/metabolism ; Receptors, Opioid/classification ; Receptors, Opioid/drug effects ; Receptors, Opioid/metabolism ; Reinforcement (Psychology) ; Reward ; Substance-Related Disorders/drug therapy ; Substance-Related Disorders/metabolism ; Substance-Related Disorders/psychology
Chemical Substances	Endorphins ; Opioid Peptides ; Receptors, Opioid ; Ethanol (3K9958V90M) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2003-10-21
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2064823-6
ISSN	1873-4294 ; 1568-0266
ISSN (online)	1873-4294
ISSN	1568-0266
DOI	10.2174/1568026043451573
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Article: Influence of the endogenous opioid system on high alcohol consumption and genetic predisposition to alcoholism.

Gianoulakis, C

Journal of psychiatry & neuroscience : JPN

2001 Volume 26, Issue 4, Page(s) 304–318

Abstract: There is increasing evidence supporting a link between the endogenous opioid system and excessive alcohol consumption. Acute or light alcohol consumption stimulates the release of opioid peptides in brain regions that are associated with reward and ... ...

Abstract	There is increasing evidence supporting a link between the endogenous opioid system and excessive alcohol consumption. Acute or light alcohol consumption stimulates the release of opioid peptides in brain regions that are associated with reward and reinforcement and that mediate, at least in part, the reinforcing effects of ethanol. However, chronic heavy alcohol consumption induces a central opioid deficiency, which may be perceived as opioid withdrawal and may promote alcohol consumption through the mechanisms of negative reinforcement. The role of genetic factors in alcohol dependency is well recognized, and there is evidence that the activity of the endogenous opioid system under basal conditions and in response to ethanol may play a role in determining an individual's predisposition to alcoholism. The effectiveness of opioid receptor antagonists in decreasing alcohol consumption in people with an alcohol dependency and in animal models lends further support to the view that the opioid system may regulate, either directly or through interactions with other neurotransmitters, alcohol consumption. A better understanding of the complex interactions between ethanol, the endogenous opioids and other neurotransmitter systems will help to delineate the neurochemical mechanisms leading to alcoholism and may lead to the development of novel treatments.
MeSH term(s)	Alcohol Drinking/genetics ; Alcohol Drinking/physiopathology ; Alcoholism/genetics ; Alcoholism/physiopathology ; Animals ; Disease Models, Animal ; Endorphins/physiology ; Genetic Predisposition to Disease/genetics ; Humans ; Models, Genetic ; Motivation ; Rats ; Receptors, Opioid/genetics ; Receptors, Opioid/physiology
Chemical Substances	Endorphins ; Receptors, Opioid
Language	English
Publishing date	2001-10-01
Publishing country	Canada
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1077443-9
ISSN	1180-4882
ISSN	1180-4882
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Article ; Online: Effects of corticotropin-releasing hormone receptor antagonists on the ethanol-induced increase of dynorphin A1-8 release in the rat central amygdala.

Lam, Minh P / Gianoulakis, Christina

Alcohol (Fayetteville, N.Y.)

2011 Volume 45, Issue 7, Page(s) 621–630

Abstract: Neurons in the central amygdala (CeA) co-express dynorphin and corticotropin-releasing hormone (CRH). Moreover, the activity of both the CRH and dynorphin systems in CeA is altered by alcohol treatments, effects suggesting interactions between the CRH ... ...

Abstract	Neurons in the central amygdala (CeA) co-express dynorphin and corticotropin-releasing hormone (CRH). Moreover, the activity of both the CRH and dynorphin systems in CeA is altered by alcohol treatments, effects suggesting interactions between the CRH and dynorphin systems. Thus, the objectives of the present study were to investigate the effects of (1) activating CRH receptors (CRHRs) by microinjection of CRH in CeA and (2) blocking CRHRs by local microinjections of CRHR antagonists in the CeA on the alcohol-induced changes in the extracellular concentrations of dynorphin A1-8 with in vivo microdialysis experiments. Microdialysis probes with a microinjection port were implanted in the CeA of alcohol-naïve Sprague-Dawley rats. Microinjections of CRH or antalarmin, a CRH receptor type 1 (CRHR1) antagonist, or anti-sauvagine-30, a CRH receptor type 2 (CRHR2) antagonist, at the level of CeA were followed by an intraperitoneal injection of either saline or 2.8 g ethanol/kg body weight. The content of dynorphin A1-8 was determined in dialyzate samples obtained prior to and following the various treatments using a specific radioimmunoassay. Activation of CRHRs in CeA induced an increase in the extracellular concentrations of dynorphin A1-8. Moreover, acute alcohol administration increased the extracellular concentrations of dynorphin A1-8 in CeA, an effect that was attenuated by blocking CRHR2 with anti-sauvagine-30 microinjection but not blocking CRHR1 with antalarmin microinjection. Therefore, the findings suggest an interaction between the CRH and dynorphin A1-8 systems at the level of CeA in response to acute alcohol exposure.
MeSH term(s)	Amphibian Proteins/antagonists & inhibitors ; Amygdala/drug effects ; Amygdala/secretion ; Animals ; Corticotropin-Releasing Hormone/pharmacology ; Dynorphins/secretion ; Ethanol/pharmacology ; Male ; Microdialysis ; Microinjections ; Peptide Fragments/secretion ; Peptide Hormones/antagonists & inhibitors ; Pyrimidines/pharmacology ; Pyrroles/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Corticotropin-Releasing Hormone/antagonists & inhibitors ; Receptors, Corticotropin-Releasing Hormone/physiology
Chemical Substances	Amphibian Proteins ; Peptide Fragments ; Peptide Hormones ; Pyrimidines ; Pyrroles ; Receptors, Corticotropin-Releasing Hormone ; antalarmin ; Ethanol (3K9958V90M) ; sauvagine (74434-59-6) ; Dynorphins (74913-18-1) ; dynorphin (1-8) (75790-53-3) ; Corticotropin-Releasing Hormone (9015-71-8)
Language	English
Publishing date	2011-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605912-0
ISSN	1873-6823 ; 0741-8329
ISSN (online)	1873-6823
ISSN	0741-8329
DOI	10.1016/j.alcohol.2011.05.001
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Article ; Online: Effects of acute ethanol on corticotropin-releasing hormone and β-endorphin systems at the level of the rat central amygdala.

Lam, Minh P / Gianoulakis, Christina

Psychopharmacology

2011 Volume 218, Issue 1, Page(s) 229–239

Abstract: Rationale: The endogenous opioid and corticotropin-releasing hormone (CRH) systems, present in the central amygdala (CeA), are implicated in alcohol consumption.: Objectives: The purpose of this study is to investigate the hypothesis that, in CeA, ... ...

Abstract	Rationale: The endogenous opioid and corticotropin-releasing hormone (CRH) systems, present in the central amygdala (CeA), are implicated in alcohol consumption. Objectives: The purpose of this study is to investigate the hypothesis that, in CeA, alcohol stimulates CRH release, which then stimulates β-endorphin release. Materials and methods: Rats were unilaterally implanted with a guide cannula to aim microdialysis probes in CeA. Experiment 1: rats received an intraperitoneal (IP) injection of various ethanol doses (0.0, 2.0, 2.4, or 2.8 g ethanol/kg body weight) and microdialysates were sampled at 30-min intervals to determine the effects over time of acute alcohol on the extracellular CRH concentrations in CeA. Experiment 2: phosphate-buffered saline, CRH, or CRH receptor (CRHR) antagonists (antalarmin or anti-sauvagine-30) was microinjected into CeA followed by a saline or 2.8 g/kg ethanol IP injection to determine the effects of CRHR activation or blockade in CeA on the basal and alcohol-stimulated release of β-endorphin. CRH and β-endorphin dialysate contents were determined using specific radioimmunoassays. Results: Acute alcohol induced a delayed increase in the extracellular CRH levels in CeA. Behavioural data showed no difference in locomotion between alcohol- and saline-treated rats. However, a transient increase in grooming was observed which did not correspond with alcohol-induced changes in CRH. Local CRH microinjections increased the extracellular β-endorphin concentrations in CeA. CRHR1 and CRHR2 blockade with microinjections of antalarmin and anti-sauvagine-30, respectively, attenuated the alcohol-induced increase of extracellular β-endorphin in CeA. Conclusions: Acute alcohol exerts indirect actions on CRH release and induced interactions of the CRH and β-endorphin systems in CeA.
MeSH term(s)	Amygdala/drug effects ; Amygdala/metabolism ; Animals ; Behavior, Animal/drug effects ; Corticotropin-Releasing Hormone/administration & dosage ; Corticotropin-Releasing Hormone/drug effects ; Corticotropin-Releasing Hormone/metabolism ; Dose-Response Relationship, Drug ; Ethanol/administration & dosage ; Ethanol/pharmacology ; Injections, Intraperitoneal ; Male ; Microdialysis ; Microinjections ; Peptide Fragments/pharmacology ; Pyrimidines/pharmacology ; Pyrroles/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Corticotropin-Releasing Hormone/drug effects ; Receptors, Corticotropin-Releasing Hormone/metabolism ; beta-Endorphin/drug effects ; beta-Endorphin/metabolism
Chemical Substances	Peptide Fragments ; Pyrimidines ; Pyrroles ; Receptors, Corticotropin-Releasing Hormone ; antalarmin ; antisauvagine 30 ; Ethanol (3K9958V90M) ; beta-Endorphin (60617-12-1) ; Corticotropin-Releasing Hormone (9015-71-8)
Language	English
Publishing date	2011-05-20
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	130601-7
ISSN	1432-2072 ; 0033-3158
ISSN (online)	1432-2072
ISSN	0033-3158
DOI	10.1007/s00213-011-2337-x
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Article: Implications of endogenous opioids and dopamine in alcoholism: human and basic science studies.

Gianoulakis, C

Alcohol and alcoholism (Oxford, Oxfordshire). Supplement

1996 Volume 31, Issue 1, Page(s) 33–42

Abstract: We investigated the endogenous opioid system and its role in mediating the reinforcing effects of ethanol that lead to high ethanol consumption as a biochemical marker of an individual's vulnerability to excessive ethanol consumption. We performed ... ...

Abstract	We investigated the endogenous opioid system and its role in mediating the reinforcing effects of ethanol that lead to high ethanol consumption as a biochemical marker of an individual's vulnerability to excessive ethanol consumption. We performed studies using human subjects with [high risk (HR)] and without [low risk (LR)] a family history of alcoholism to supplement our studies with experimental animals bred selectively for high- or low-ethanol consumption. HR subjects had lower basal plasma beta-endorphin levels as compared with LR subjects, but they had a more pronounced release of beta-endorphin after exposure to ethanol. Findings from animal studies indicated that ethanol-preferring (C57BL/6) mice (analogous to the HR human subjects) had higher levels of hypothalamic beta-endorphin activity than did ethanol-avoiding (DBA/2) mice (analogous to the LR human subjects) under basal conditions. However, the C57BL/6 mice had a more pronounced release of hypothalamic beta-endorphin than did DBA/2 mice after exposure to ethanol. Thus, although hypothalamic beta-endorphin system activity in human and animal models of alcoholism differs under basal conditions, there is enhanced hypothalamic beta-endorphin system activity after exposure to ethanol in both models. We have also performed studies comparing the density and distribution of opioid receptors in brains of ethanol-preferring animals, such as C57BL/6 mice and ALKO-alcohol (AA) rats, and ethanol-avoiding animals, such as DBA/2 mice and ALKO-non-alcohol (ANA) rats. Interestingly, it was observed that in distinct brain regions known to be important for mediating the process of reinforcement, the C57BL/6 mice had a higher density of delta-opioid receptors than the DBA/2 mice, while the AA rats had a higher density of mu-opioid receptors than the ANA rats. Thus, in the ethanol-preferring animals, the increased release of beta-endorphin following exposure to ethanol was associated with a higher density of delta- or mu-opioid receptors in brain regions important for reinforcement, such as the nucleus accumbens and the ventral tegmental area, and may interact with the dopaminergic system and promote ethanol's reinforcing properties, leading to excessive drinking and alcoholism.
MeSH term(s)	Alcoholism/genetics ; Alcoholism/physiopathology ; Alcoholism/psychology ; Animals ; Brain/physiopathology ; Dopamine/physiology ; Endorphins/physiology ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Models, Neurological ; Rats ; Reinforcement (Psychology)
Chemical Substances	Endorphins ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	1996-03
Publishing country	England
Document type	Journal Article ; Review
ISSN	1358-6173
ISSN	1358-6173
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Article: Implications of endogenous opioids and dopamine in alcoholism: human and basic science studies.

Gianoulakis, C

Alcohol and alcoholism (Oxford, Oxfordshire)

1996 Volume 31 Suppl 1, Page(s) 33–42

Abstract	We investigated the endogenous opioid system and its role in mediating the reinforcing effects of ethanol that lead to high ethanol consumption as a biochemical marker of an individual's vulnerability to excessive ethanol consumption. We performed studies using human subjects with [high risk (HR)] and without [low risk (LR)] a family history of alcoholism to supplement our studies with experimental animals bred selectively for high- or low-ethanol consumption. HR subjects had lower basal plasma beta-endorphin levels as compared with LR subjects, but they had a more pronounced release of beta-endorphin after exposure to ethanol. Findings from animal studies indicated that ethanol-preferring (C57BL/6) mice (analogous to the HR human subjects) had higher levels of hypothalamic beta-endorphin activity than did ethanol-avoiding (DBA/2) mice (analogous to the LR human subjects) under basal conditions. However, the C57BL/6 mice had a more pronounced release of hypothalamic beta-endorphin than did DBA/2 mice after exposure to ethanol. Thus, although hypothalamic beta-endorphin system activity in human and animal models of alcoholism differs under basal conditions, there is enhanced hypothalamic beta-endorphin system activity after exposure to ethanol in both models. We have also performed studies comparing the density and distribution of opioid receptors in brains of ethanol-preferring animals, such as C57BL/6 mice and ALKO-alcohol (AA) rats, and ethanol-avoiding animals, such as DBA/2 mice and ALKO-non-alcohol (ANA) rats. Interestingly, it was observed that in distinct brain regions known to be important for mediating the process of reinforcement, the C57BL/6 mice had a higher density of delta-opioid receptors than the DBA/2 mice, while the AA rats had a higher density of mu-opioid receptors than the ANA rats. Thus, in the ethanol-preferring animals, the increased release of beta-endorphin following exposure to ethanol was associated with a higher density of delta- or mu-opioid receptors in brain regions important for reinforcement, such as the nucleus accumbens and the ventral tegmental area, and may interact with the dopaminergic system and promote ethanol's reinforcing properties, leading to excessive drinking and alcoholism.
MeSH term(s)	Alcoholism/genetics ; Alcoholism/physiopathology ; Animals ; Brain/physiopathology ; Brain Mapping ; Dopamine/physiology ; Double-Blind Method ; Ethanol/pharmacokinetics ; Female ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Neural Pathways/physiopathology ; Opioid Peptides/physiology ; Rats ; Risk Factors ; Selection, Genetic ; beta-Endorphin/physiology
Chemical Substances	Opioid Peptides ; Ethanol (3K9958V90M) ; beta-Endorphin (60617-12-1) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	1996-03
Publishing country	England
Document type	Clinical Trial ; Journal Article ; Randomized Controlled Trial
ZDB-ID	604956-4
ISSN	1464-3502 ; 0735-0414 ; 0309-1635
ISSN (online)	1464-3502
ISSN	0735-0414 ; 0309-1635
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Article ; Online: Cortisol stress response predicts 9-year risky driving convictions in male first-time driving-while-impaired offenders.

Brown, Thomas G / Ouimet, Marie Claude / Nadeau, Louise / Tremblay, Jacques / Gianoulakis, Christina / Couture, Sophie / Moxley-Kelly, Nathaniel

Psychopharmacology

2019 Volume 237, Issue 1, Page(s) 177–187

Abstract: Background: With driving while impaired by alcohol (DWI) representing a persistent burden on global health, better understanding and prevention of recidivism following a first-time DWI conviction are needed. Progress towards these goals is challenged by ...

Abstract	Background: With driving while impaired by alcohol (DWI) representing a persistent burden on global health, better understanding and prevention of recidivism following a first-time DWI conviction are needed. Progress towards these goals is challenged by the marked heterogeneity in offender characteristics and a traffic safety literature that relies on subjective self-report measures and cross-sectional study designs. The present study tested the hypothesis that an objective neurobiological marker of behavioural maladjustment, the cortisol stress response (CSR), predicts future DWI and other traffic convictions over a 9-year follow-up period. Methods: One hundred thirty-two male first-time DWI offenders and 31 non-offender comparators were recruited and assessed at intake for their substance use, psychosocial and psychological characteristics and CSR. Traffic conviction data were obtained from provincial driving records. Survival analysis estimated the association between CSR and risk of a traffic conviction over time. Results: In support of our hypothesis, blunted CSR predicted traffic convictions during the follow-up duration. This effect generalized to both DWI offenders and non-DWI drivers. While CSR was lower in DWI offenders compared to non-offenders, it did not specifically predict recidivism in DWI offenders. Modelling results indicated that blunted CSR, along with DWI offender group membership, experience seeking and drug use frequency, may demarcate a high-risk driver phenotype. Conclusions: CSR is a neurobiological marker of a driver phenotype with elevated generalized driving risk. For drivers with characteristics consistent with this phenotype, expanding the focus of intervention to address multiple forms of risky driving may be necessary to curb their overall threat to traffic safety.
MeSH term(s)	Adult ; Alcoholic Intoxication/physiopathology ; Criminals ; Cross-Sectional Studies ; Driving Under the Influence/legislation & jurisprudence ; Driving Under the Influence/physiology ; Humans ; Hydrocortisone/analysis ; Male ; Saliva/chemistry ; Young Adult
Chemical Substances	Hydrocortisone (WI4X0X7BPJ)
Language	English
Publishing date	2019-09-11
Publishing country	Germany
Document type	Journal Article
ZDB-ID	130601-7
ISSN	1432-2072 ; 0033-3158
ISSN (online)	1432-2072
ISSN	0033-3158
DOI	10.1007/s00213-019-05359-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

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