Prolonged Exposure to Intermittent Alcohol Vapors Blunts Hypothalamic Responsiveness to Immune and Non‐Immune Signals

Lee, Soon; Schmidt, Donne; Tilders, F. J. H.; Cole, Maury; Smith, Amanda; Rivier, Catherine

doi:10.1111/j.1530-0277.2000.tb04560.x

Cited by 61 publications

(40 citation statements)

References 77 publications

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“…During the development of ethanol dependence, both hypothalamic as well as extrahypothalamic CRF systems become dysregulated. In rats, acute ethanol activates the HPA axis (Rivier et al 1984), while chronic exposure to ethanol, as well as ethanol withdrawal, leads to an attenuation of HPA axis activity (Dave et al 1986;Lee et al 2000;Rivier et al 1990;Zorrilla et al 2001). In contrast, extrahypothalamic CRF systems become hyperactive during withdrawal from chronic ethanol exposure.…”

Section: Discussionmentioning

confidence: 99%

Corticotropin-Releasing Factor 1 Antagonists Selectively Reduce Ethanol Self-Administration in Ethanol-Dependent Rats

Funk

Zorrilla

Lee

et al. 2007

Biological Psychiatry

262

242

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Background-Alcohol dependence is characterized by excessive alcohol consumption, loss of control over intake, and the presence of a withdrawal syndrome, which includes both motivational and physical symptoms. Similar to human alcoholics, ethanol-dependent animals display enhanced anxiety-like behaviors and enhanced ethanol self-administration during withdrawal, effects hypothesized to result from a dysregulation of corticotropin-releasing factor (CRF) stress systems. Here, we used an animal model of ethanol dependence to test the effects of CRF 1 receptor antagonists on excessive ethanol self-administration in dependent rats.

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Section: Discussionmentioning

confidence: 99%

Corticotropin-Releasing Factor 1 Antagonists Selectively Reduce Ethanol Self-Administration in Ethanol-Dependent Rats

Funk

Zorrilla

Lee

et al. 2007

Biological Psychiatry

262

242

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“…Fetal alcohol exposure affects HPA axis activity through changes in the hypothalamus and brain areas that are functionally connected to the hypothalamus [91], with the result that HPA tone is increased throughout the lifespan [71], though to a greater extent in males than in females. A number of laboratories have found no difference between males and females exposed to fetal alcohol in the stimulated release of adrenocorticotropin-releasing hormone [92][93][94], which would suggest that the hypersensitivity to stress that the animals express is the result of altered negative feedback in the brain. In fact, fetal alcohol exposure dysregulates the 'stress axis' by altering gene expression including pituitary pro-opiomelanocortin gene transcripts and beta-endorphin expression in the brain [77,95,96], both of which are changed to a greater extent in males than in females.…”

Section: Alcoholmentioning

confidence: 99%

An examination of sex differences in the effects of early-life opiate and alcohol exposure

Terasaki¹,

Gomez²,

Schwarz³

2016

Phil. Trans. R. Soc. B

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One contribution of 16 to a theme issue 'Multifaceted origins of sex differences in the brain'. Early-life exposure to drugs and alcohol is one of the most preventable causes of developmental, behavioural and learning disorders in children. Thus a significant amount of basic, animal and human research has focused on understanding the behavioural consequences and the associated neural effects of exposure to drugs and alcohol during early brain development. Despite this, much of the previous research that has been done on this topic has used predominantly male subjects or rodents. While many of the findings from these male-specific studies may ultimately apply to females, the purpose of this review is to highlight the research that has also examined sex as a factor and found striking differences between the sexes in their response to early-life opiate and alcohol exposure. Finally, we will also provide a framework for scientists interested in examining sex as a factor in future experiments that specifically examine the consequences of early-life drug and alcohol exposure.

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“…The inhalation chamber has the advantage of easily achieving and maintaining the targeted blood alcohol level (BAL) (Kliethermes et al, 2004). Moreover, the variability in the ethanol concentration between similarly controlled chambers is minimal Lee et al, 2000).…”

Section: Vapor Ethanol Exposure and Drug Treatmentmentioning

confidence: 99%

Desipramine blocks alcohol-induced anxiety- and depressive-like behaviors in two rat strains☆

Getachew¹,

Hauser²,

Taylor³

et al. 2008

Pharmacology Biochemistry and Behavior

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Epidemiological studies indicate significant co-morbid expression of alcoholism, anxiety, and depression. These symptoms are often under-diagnosed and under-treated and can worsen prognostic and treatment outcome for alcoholism. Nonetheless, a causal relationship between alcoholism and these conditions is yet to be established. In this study we sought to determine the effects of daily alcohol administration on the indices of anxiety and depression in two rat strains, one of which exhibits inherent depressive-like characteristics. Moreover, it was of relevance to examine the effects of a clinically useful antidepressant on alcohol-induced behavioral changes. Wistar-Kyoto (WKY) rats derived from Wistar stock show low levels of locomotor activity in an open field and high levels of immobility in the forced swim test (FST) which is considered a measure of their helplessness and hence are considered a putative animal model of depression. Adult female WKY and Wistar rats were exposed for 3 hrs daily to 95% ethanol vapor to achieve a mean blood alcohol level (BAL) of approximately 150 mg/dL. Controls were exposed to air in similar inhalation chambers. Sixteen to 18 hrs following 7 or 14 days of exposure to alcohol, locomotor activity (LCA) in open field, duration of time spent in the open arm of the elevated plus-maze (EPM), reflective of anxiety-like behavior and immobility in FST were evaluated. Alcohol exposure for 7 or 14 days reduced LCA only in Wistar rats but enhanced FST immobility in both strains at both time points. Only 14 day alcohol exposure reduced EPM open arm time in both WKY and Wistar rats. Daily treatment with desipramine (8 mg/kg) blocked all the changes induced by alcohol in both strains. Thus, subchronic (7 day) exposure to alcohol induces depressive-like characteristics in Wistar rats and exacerbates that of WKY rats. Chronic (14 day) exposure, however, also induces an anxiety-like effect in both strains. The depressive-and anxietylike behaviors induced by alcohol were blocked by daily treatment with a tricyclic antidepressant. It may be suggested that prophylactic treatment of alcoholics with an antidepressant prior to detoxification may improve treatment outcome for alcoholism.

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Prolonged Exposure to Intermittent Alcohol Vapors Blunts Hypothalamic Responsiveness to Immune and Non‐Immune Signals

Cited by 61 publications

References 77 publications

Corticotropin-Releasing Factor 1 Antagonists Selectively Reduce Ethanol Self-Administration in Ethanol-Dependent Rats

Corticotropin-Releasing Factor 1 Antagonists Selectively Reduce Ethanol Self-Administration in Ethanol-Dependent Rats

An examination of sex differences in the effects of early-life opiate and alcohol exposure

Desipramine blocks alcohol-induced anxiety- and depressive-like behaviors in two rat strains☆

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