Effects of Ethanol on CRF Release<i>in Vitro</i>*

Redei, Eva E.; Branch, Berrilyn J.; Gholami, Saeed; Lin, Eric Y; Taylor, Anna N.

doi:10.1210/endo-123-6-2736

Cited by 66 publications

(22 citation statements)

References 41 publications

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“…These findings suggest that alcohol may directly activate HPA axis through regulating the PVN cellular activity. Indeed, in vitro application of alcohol to hypothalamic tissue or primary hypothalamic cells induces the release of CRF (Redei et al, 1988; Li et al, 2005). In addition, CRF heteronuclear RNA quickly elevates within 20 min after in vivo alcohol administration in rats (Rivier and Lee, 1996; Ogilvie et al, 1998).…”

Section: Alcohol Stimulates the Release Of Stress Hormonesmentioning

confidence: 99%

Alcohol, stress hormones, and the prefrontal cortex: A proposed pathway to the dark side of addiction

Richardson

2014

Neuroscience

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Chronic exposure to alcohol produces changes in the prefrontal cortex that are thought to contribute to the development and maintenance of alcoholism. A large body of literature suggests that stress hormones play a critical role in this process. Here we review the bi-directional relationship between alcohol and stress hormones, and discuss how alcohol acutely stimulates the release of glucocorticoids and induces enduring modifications to neuroendocrine stress circuits during the transition from non-dependent drinking to alcohol dependence. We propose a pathway by which alcohol and stress hormones elicit neuroadaptive changes in prefrontal circuitry that could contribute functionally to a dampened neuroendocrine state and the increased propensity to relapse—a spiraling trajectory that could eventually lead to dependence.

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Section: Alcohol Stimulates the Release Of Stress Hormonesmentioning

confidence: 99%

Alcohol, stress hormones, and the prefrontal cortex: A proposed pathway to the dark side of addiction

Richardson

2014

Neuroscience

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“…Acute ethanol administration is accompanied by increases in levels of CRF [18] and CRF-like immunoreactivity (CRF-IR) [19], as well as increased levels of CRF heteronuclear RNA (hnRNA) and messenger RNA (mRNA) [18, 20, 21] in the hypothalamus. Acute ethanol administration also induces activation of Ucn-positive cells in the perioculomotor urocortin-containing population of neurons (pIIIu, also known as the Edinger-Westphal nucleus) [22].…”

Section: The Effects Of Ethanol On the Crf/ucn Systemmentioning

confidence: 99%

Pre-Clinical Evidence that Corticotropin-Releasing Factor (CRF) Receptor Antagonists are Promising Targets for Pharmacological Treatment of Alcoholism

Lowery¹,

Thiele²

2010

CNSNDDT

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Alcoholism is a chronic disorder characterized by cycling periods of excessive ethanol consumption, withdrawal, abstinence and relapse, which is associated with progressive changes in central corticotropin-releasing factor (CRF) receptor signaling. CRF and urocortin (Ucn) peptides act by binding to the CRF type 1 (CRF1R) or the CRF type 2 (CRF2R) receptors, both of which have been implicated in the regulation of neurobiological responses to ethanol. The current review provides a comprehensive overview of preclinical evidence from studies involving rodents that when viewed together, suggest a promising role for CRF receptor (CRFR) antagonists in the treatment of alcohol abuse disorders. CRFR antagonists have been shown to protect against excessive ethanol intake resulting from ethanol dependence without influencing ethanol intake in non-dependent animals. Similarly, CRFR antagonists block excessive binge-like ethanol drinking in non-dependent mice but do not alter ethanol intake in mice drinking moderate amounts of ethanol. CRFR antagonists protect against increased ethanol intake and relapse-like behaviors precipitated by exposure to a stressful event. Additionally, CRFR antagonists attenuate the negative emotional responses associated with ethanol withdrawal. The protective effects of CRFR antagonists are modulated by the CRF1R. Finally, recent evidence has emerged suggesting that CRF2R agonists may also be useful for treating alcohol abuse disorders. KeywordsCorticotropin-releasing factor; urocortin; CRF receptor; alcoholism; dependence; withdrawal; relapse; ethanol Corticotropin-releasing factor (CRF) is a 41-amino acid poly-peptide that is widely expressed throughout the central nervous system (CNS) and modulates a range of neurobiological responses through activation of the G s -protein coupled CRF type 1 (CRF1R) and type 2 (CRF2R) receptors [1][2][3][4]. While CRF binds to both receptors, it has greater affinity to the CRF1R [1,5,6]. CRFRs are also stimulated by the 40-amino acid urocortin (Ucn) family of peptides, with Urocortin I (Ucn1) displaying equal affinity for both CRF1R and CRF2R, and Urocortin II (Ucn2) and Urocortin III (Ucn3) displaying affinity primarily for the CRF2R [1,6,7]. In rodents, expression of the CRF1R is ubiquitous throughout the brain, with high density found in hypothalamic, cortical, and limbic regions, while CRF2R expression is limited to specific regions, including the raphe nuclei, lateral septum, and subregions of the amygdala [1]. Agonist binding of these receptors induces distinct outcomes with respect to cellular signaling pathways, downstream mechanisms, and behavior [1,8,9]. CRF and Ucn signaling through CRF1Rs and CRF2Rs have been implicated in a number of biobehavioral processes, including regulation of the hypothalamic-pituitary-adrenal (HPA) axis stress response, anxiety, depression, feeding, and excessive alcohol consumption [1,3,6,[10][11][12][13][14].Alcoholism is a chronic and progressive disorder characterized by cyclic patterns of excessive ethanol sel...

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“…In addition to its centrally mediated hypothermic effects, EtOH exposure activates the hypothalamic-pituitary-adrenal (HPA) axis (Redei et al, 1986(Redei et al, , 1988Rivier and Lee, 1996). Studies have also shown that alcohol generally suppresses the hypothalamic-pituitary-gonadotropin axes of animals and humans (Cicero and Badger, 1977;Mendelson et al, 1977;Rivier, 1999).…”

Section: Discussionmentioning

confidence: 99%

Sex Differences in Ethanol‐Induced Hypothermia in Ethanol‐Naïve and Ethanol‐Dependent/Withdrawn Rats

Taylor¹,

Tio²,

Bando³

et al. 2008

Alcoholism Clin & Exp Res

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Background: Human and animal findings indicate that males and females display major differences in risk for and consequences of alcohol abuse and alcoholism. These differences are in large part mediated by sex-specific hormonal environments. Gonadal and adrenal secretory products are known to modulate the neurobehavioral responses of ethanol (EtOH) dependence and withdrawal. However, the effects of these steroids on physiological adaptations, such as thermoregulation, are less well established. To study the role of sex-related hormones in mediating sex differences in the hypothermic response to acute challenge with EtOH, we compared the EtOHinduced hypothermic responses of EtOH-naı¨ve male and female rats and EtOH-dependent (on the third day of withdrawal) male and female rats before (intact) and after depletion of all gonadal and adrenal steroids by gonadectomy (GDX) with or without adrenalectomy (ADX).Methods: Intact and GDX male and female rats, with or without ADX, were fed an EtOHcontaining liquid diet for 15 days while control (EtOH-naı¨ve) rats were pairfed the isocaloric liquid diet without EtOH or fed normal rat chow and water. On the third day of withdrawal from the EtOH diet we tested the hypothermic response to EtOH challenge (1.5 g ⁄ kg BWt, ip). Blood alcohol content (BAC) and corticosterone (CORT) content were analyzed in a separate series of intact and GDX males and females with and without ADX in response to the EtOH challenge.Results: Ethanol-induced hypothermia was significantly greater and its duration significantly longer in intact males than females when subjects were EtOH-naı¨ve. EtOH-induced hypothermia was significantly greater in intact females than males by the third day of withdrawal from EtOH dependence. GDX in males significantly shortened the duration of the hypothermic response and tended to blunt EtOH-induced hypothermia while response duration was significantly extended by GDX in females that tended to enhance EtOH-hypothermia. EtOH-induced hypothermia was significantly enhanced and its duration significantly lengthened by combined GDX and ADX in EtOH-naı¨ve and -withdrawn males and by combined GDX and ADX in EtOH-naı¨ve but not EtOH-withdrawn females. These differential EtOH-induced hypothermic responses did not appear to be caused by differences in EtOH handling among the groups. The absence of adrenal activation by EtOH in the GDX-ADX males and females contributes to their enhanced EtOH-induced hypothermic responses.Conclusions: These results implicate the direct and indirect effects of removal of gonadal and adrenal secretory products as mediators of the thermoregulatory actions of EtOH.

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Effects of Ethanol on CRF Releasein Vitro*

Cited by 66 publications

References 41 publications

Alcohol, stress hormones, and the prefrontal cortex: A proposed pathway to the dark side of addiction

Alcohol, stress hormones, and the prefrontal cortex: A proposed pathway to the dark side of addiction

Pre-Clinical Evidence that Corticotropin-Releasing Factor (CRF) Receptor Antagonists are Promising Targets for Pharmacological Treatment of Alcoholism

Sex Differences in Ethanol‐Induced Hypothermia in Ethanol‐Naïve and Ethanol‐Dependent/Withdrawn Rats

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