Role of exercise in the treatment of alcohol use disorders.

Excessive alcohol use can cause harmful effects on the human body, which are associated with serious health problems, and it can also lead to the development of alcohol use disorders (AUDs). There is certain evidence that physical exercise positively affects excessive alcohol use and the associated problems by leading to reduced alcohol intake. A literature search was conducted using the databases PubMed, Medline and Web of Science.

Lower Cortisol Activity is Associated with First-Time Driving while Impaired.

Driving while impaired (DWI) is a grave and persistent high-risk behavior. Previous work demonstrated that DWI recidivists had attenuated cortisol reactivity compared to non-DWI drivers. This suggests that cortisol is a neurobiological marker of high-risk driving.

Higher crash and near-crash rates in teenaged drivers with lower cortisol response: an 18-month longitudinal, naturalistic study.

Importance: Road traffic crashes are one of the leading causes of injury and death among teenagers worldwide. Better understanding of the individual pathways to driving risk may lead to better-targeted intervention in this vulnerable group.

Objective: To examine the relationship between cortisol, a neurobiological marker of stress regulation linked to risky behavior, and driving risk.

Effects of corticotropin-releasing hormone receptor antagonists on the ethanol-induced increase of dynorphin A1-8 release in the rat central amygdala.

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.

Effects of acute ethanol on corticotropin-releasing hormone and β-endorphin systems at the level of the rat central amygdala.

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.

The effect of naltrexone on alcohol's stimulant properties and self-administration behavior in social drinkers: influence of gender and genotype.

Background: Few pharmacological treatments for alcohol dependence are available. Moreover, the best supported treatment, naltrexone hydrochloride, appears to work for only some.

Methods: To investigate potential predictors of these differential responses, 40 social drinkers (20 women) were administered 6 days of treatment with naltrexone vs.

Effects of acute ethanol on beta-endorphin release in the nucleus accumbens of selectively bred lines of alcohol-preferring AA and alcohol-avoiding ANA rats.

Rationale: The selectively bred lines of alcohol-preferring alko alcohol (AA) and alcohol-avoiding alko nonalcohol (ANA) rats have been used to demonstrate differences in relevant neurotransmitters which could account for their difference in alcohol consumption. Studies have demonstrated differences in distinct components of the endogenous opioid system in various brain regions associated with the process of reinforcement between the AA and ANA lines of rats.

Objectives: The goal of this current study was to investigate the hypotheses that the AA and ANA rats will show differences in the release of beta-endorphin at the level of nucleus accumbens (NAC) and in locomotor activity in response to acute systemic administration of ethanol.

Endogenous opioids and addiction to alcohol and other drugs of abuse.

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.

From the brain to bad behaviour and back again: neurocognitive and psychobiological mechanisms of driving while impaired by alcohol.

Issues: Driving while impaired by alcohol (DWI) is responsible for substantial mortality and injury. Significant gaps in our understanding of DWI re-offending, or recidivism, reduce our ability to practically assess recidivism probability and to match interventions to individual risk profiles. These shortcomings reflect the baffling heterogeneity in the DWI population and the limited focus of much existing DWI recidivism research to psychosocial, psychological and substance use correlates.

Effect of acute ethanol administration on the release of opioid peptides from the midbrain including the ventral tegmental area.

Background: Experimental evidence suggests that ethanol alters the activity of the endogenous opioid peptide systems in a dose and brain-region dependent manner. These alterations may influence the processes of ethanol reward and reinforcement. Thus, it was the objective of this study to investigate the response of the 3 major opioid peptide systems (endorphins, enkephalins, and dynorphins) to acute ethanol administration, at the level of the midbrain including the ventral tegmental area (midbrain/VTA), a region important for drug, including ethanol reinforcement.

Effects of acute ethanol on opioid peptide release in the central amygdala: an in vivo microdialysis study.

Rationale: There is experimental evidence that indicates that the endogenous opioid system of the central nucleus of the amygdala (CeA) may mediate some of the reinforcing effects of ethanol. However, the precise interactions of ethanol with the endogenous opioid system at the level of the CeA have not been investigated.

Objectives: The aim of the current study was to investigate the hypothesis that acute systemic ethanol administration will increase the release of endogenous opioid peptides at the level of the CeA in a time- and dose-dependent manner.

Hypothalamic-pituitary-adrenal axis response to stress in male DUI recidivists.

Cortisol is a stress hormone mediated by the hypothalamic-pituitary-adrenal (HPA) axis and a psychobiological marker of genetic risk for alcoholism and other high-risk behavioural characteristics. In previous work with driving under the influence of alcohol (DUI) recidivists, we uncovered a significant inverse relationship between the frequency of past DUI convictions and salivary cortisol, whose strength surpassed those observed between DUI frequency and measures of alcohol abuse and other DUI-related characteristics. This finding emerged using a methodology not specifically contrived to test this relationship.

Response of the HPA-axis to alcohol and stress as a function of alcohol dependence and family history of alcoholism.

Dysfunction of the hypothalamic-pituitary-adrenal (HPA)-axis has been observed in chronic alcoholics and in non-alcoholic sons of alcoholic parents, while genetic and environmental factors, such as stress, may play a significant role in the development of alcoholism. The present study was designed to investigate the response of the HPA-axis to alcohol and stress as a function of family history of alcoholism and chronic alcohol abuse. We determined changes in plasma adrenal corticotrophin (ACTH) and cortisol concentrations in response to a placebo or an alcohol (0.

Neurocognitive characteristics of DUI recidivists.

Individuals who drive under the influence (DUI) of alcohol may be at greater risk for neurocognitive impairment because of their exposure to multiple sources of neurological risk. This could contribute to the persistence of DUI behaviour and influence the effectiveness of remedial interventions. The objectives of this study were to clarify the neurocognitive characteristics of DUI recidivists and the nature of potential impairments, and to explore relationships between these characteristics and the frequency of past DUI convictions.

Differential effects of naltrexone on cardiac, subjective and behavioural reactions to acute ethanol intoxication.

Objective: Alcohol may have psychomotor stimulant properties during the rising limb of the blood alcohol curve at commonly self-administered doses. Increased heart rate (HR) immediately after alcohol consumption may serve as an indicator or marker of such properties, which appear to be potentially opiate-mediated and dopamine-dependent. Naltrexone, an opiate antagonist, has been used successfully in the treatment of alcoholism and may produce its therapeutic effects through its effects on alcohol metabolism or by blocking alcohol's rewarding effects.

A microdialysis profile of dynorphin A(1-8) release in the rat nucleus accumbens following alcohol administration.

Background: Pharmacological studies have implicated the endogenous opioid system in mediating alcohol intake. Other evidence has shown that alcohol administration can influence endorphinergic and enkephalinergic activity, while very few studies have examined its effect on dynorphinergic systems. The aim of the present study was to investigate the effect of alcohol administration or a mechanical stressor on extracellular levels of dynorphin A(1-8) in the rat nucleus accumbens-a brain region that plays a significant role in the processes underlying reinforcement and stress.

Differences in the peripheral levels of beta-endorphin in response to alcohol and stress as a function of alcohol dependence and family history of alcoholism.

Background: Evidence indicates that both genetic and environmental factors, such as stress, may play an important role for the development of alcoholism, while beta-endorphin may be implicated in the control of alcohol consumption. The objective of the present studies was to test the hypothesis that there are differences in the response of the pituitary beta-endorphin system to stress as a function of family history of alcoholism and alcohol dependence.

Methods: The response of the pituitary beta-endorphin to a placebo or an alcohol (0.

A microdialysis profile of Met-enkephalin release in the rat nucleus accumbens following alcohol administration.

Background: Pharmacological studies have implicated the endogenous opioid system in mediating alcohol intake. Other evidence has shown that alcohol administration can influence opioid activity. In this regard, the majority of studies have concentrated on endorphinergic systems, whereas other opioid systems have been granted comparably less attention.

Levels and circadian rhythmicity of plasma ACTH, cortisol, and beta-endorphin as a function of family history of alcoholism.

Rationale: Individuals with a family history of alcoholism may present a dysfunction in the activity of the hypothalamic-pituitary-adrenal (HPA) axis that predates the development of alcoholism.

Objective: The present study investigated the hypothesis that this HPA-axis dysfunction is associated with alterations in the pattern of the circadian (24 h) secretions of adrenal corticotropic hormone (ACTH), cortisol, and beta-endorphin.

Methods: Men with [high risk (HR)] or without [low risk (LR)] family history of alcoholism participated in the study.

Salivary cortisol: a predictor of convictions for driving under the influence of alcohol?

Aims: To examine the relationship between salivary cortisol and frequency of past driving under the influence of alcohol (DUI) convictions.

Methods: A total of 104 males with previous DUI convictions (from one to eight) and mean age of 44.7 years were assessed on measures characterizing repeat DUI offenders, including sociodemographic information, alcohol use behaviours, biological indices of the organic consequences of chronic abuse, negative consequences of excessive drinking, past DUI conviction history, impulse control, and antisocial behaviour tendencies.

Endogenous opioids and addiction to alcohol and other drugs of abuse.

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.

A microdialysis profile of beta-endorphin and catecholamines in the rat nucleus accumbens following alcohol administration.

Rationale: Alcohol stimulates the release of dopamine in the nucleus accumbens (NACB) of rats, mice and humans. There is evidence to suggest that the activation of beta-endorphin (beta-EP) in the mesolimbic pathway by alcohol and other drugs of abuse may be associated with the rise in dopamine levels in the NACB.

Objectives: The present studies investigate whether the release of beta-EP in the NACB is (1) dependent on the dose of alcohol that is administered, and (2) associated with changes in the extracellular concentrations of the catecholamines dopamine and norepinephrine, and the dopamine metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), in the NACB.

Effect of chronic alcohol consumption on the activity of the hypothalamic-pituitary-adrenal axis and pituitary beta-endorphin as a function of alcohol intake, age, and gender.

Background: Experimental evidence indicates that components of the hypothalamic-pituitary-adrenal (HPA) axis and of the endogenous opioid system, such as beta-endorphin (beta-END), influence alcohol consumption, whereas chronic alcohol abuse alters the activity of both systems. Furthermore, gender and age differences have been reported in the activity of the HPA axis under basal conditions, in response to stress and acute alcohol challenge. The objective of the present studies was to investigate the hypothesis that chronic alcohol consumption alters the activity of the HPA axis and pituitary beta-END as a function of severity of alcohol abuse, gender, and age.

Estradiol valerate and alcohol intake: a comparison between Wistar and Lewis rats and the putative role of endorphins.

Studies show that estrogens can influence alcohol consumption; however, findings are variable and an etiology remains unknown. Furthermore, estrogen administration can alter several neurotransmitter systems implicated in alcohol consumption, including the beta-endorphin (beta-EP) system. The present studies investigate (a) whether estradiol valerate (EV) alters voluntary alcohol consumption in Wistar and Lewis rats, (b) if an effect of EV on drinking is associated with changes in hypothalamic or pituitary beta-EP content, and (c) whether differences in alcohol drinking between treatment and rat groups are related to locomotor or defensive behavior/anxiety scores.