Free-choice ethanol consumption by rats: effects of ACTH4–10

Krishnan, Suchitra; Nash, John J.; Maickel, Roger P.

doi:10.1016/0741-8329(91)90663-h

Cited by 23 publications

(16 citation statements)

References 23 publications

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“…For example, if considering the influence of amount of restraint stress exposure, studies have shown increased (Ploj et al 2003; Roman et al 2004), decreased (Haleem 1996; Sprague and Maickel 1994), or no change (Roman et al 2003; Tambour et al 2008) in alcohol consumption with as few as 1–4 days of restraint treatment. Similarly, studies involving more extensive restraint stress exposure (2–8 weeks) have reported increased (Derr and Lindblad 1980; Lynch et al 1999), decreased (Chester et al 2004; Krishnan et al 1991), or unaltered (Nash and Maickel 1985; Ng Cheong Ton et al 1983) alcohol intake.…”

Section: Acute/sub-chronic Stress Exposure During Alcohol Accessmentioning

confidence: 94%

“…Likewise, studies that employed relatively long durations of daily restraint (≥18 h) reported increased (Derr and Lindblad 1980) or decreased (Abraham and Gogate 1989) levels of alcohol consumption. Variable unpredictable restraint has been utilized as well, with several studies reporting decreased (Chester et al 2004; Krishnan et al 1991; Sprague and Maickel 1994) or unaltered (Nash and Maickel 1985; Rockman et al 1987) alcohol intake.…”

Section: Acute/sub-chronic Stress Exposure During Alcohol Accessmentioning

confidence: 99%

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Effects of stress on alcohol drinking: a review of animal studies

López²,

2011

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Rationale While stress is often proposed to play a significant role in influencing alcohol consumption, the relationship between stress and alcohol is complex and poorly understood. Over several decades, stress effects on alcohol drinking have been studied using a variety of animal models and experimental procedures, yet this large body of literature has generally produced equivocal results. Objectives This paper reviews results from animal studies in which alcohol consumption is evaluated under conditions of acute/sub-chronic stress exposure or models of chronic stress exposure. Evidence also is presented indicating that chronic intermittent alcohol exposure serves as a stressor that consequently influences drinking. Results The effects of various acute/sub-chronic stress procedures on alcohol consumption have generally been mixed, but most study outcomes suggest either no effect or decreased alcohol consumption. In contrast, most studies indicate that chronic stress, especially when administered early in development, results in elevated drinking later in adulthood. Chronic alcohol exposure constitutes a potent stressor itself, and models of chronic intermittent alcohol exposure reliably produce escalation of voluntary alcohol consumption. Conclusions A complex and dynamic interplay among a wide array of genetic, biological, and environmental factors govern stress responses, regulation of alcohol drinking, and the circumstances in which stress modulates alcohol consumption. Suggestions for future directions and new approaches are presented that may aid in developing more sensitive and valid animal models that not only better mimic the clinical situation, but also provide greater understanding of mechanisms that underlie the complexity of stress effects on alcohol drinking.

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Section: Acute/sub-chronic Stress Exposure During Alcohol Accessmentioning

confidence: 94%

Section: Acute/sub-chronic Stress Exposure During Alcohol Accessmentioning

confidence: 99%

Effects of stress on alcohol drinking: a review of animal studies

López²,

2011

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“…For instance, corticosterone itself has been found to be reinforcing and is self-administered by rodents orally (e.g., Deroche et al, 1993). In addition, preclinical investigations have found decreased alcohol drinking following exposure to CRF (Bell et al, 1998) and ACTH (Krishnan et al, 1991), both of which are involved in the activation of the HPA axis. Considering that increases in HPA hormones contributing to the rewarding aspects of alcohol, alcohol addicts might need to consume more alcohol to achieve the same effect after the HPA axis develops a tolerance after chronic exposure (Kreek and Koob, 1998;Koob and Kreek, 2007).…”

Section: Section I Stress Responsive Hypothalamicepituitaryeadrenal mentioning

confidence: 98%

Alcohol: A stimulant activating brain stress responsive systems with persistent neuroadaptation

Zhou

Kreek

2014

Neuropharmacology

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“…On the other hand, under certain circumstances and at certain doses, alcohol may induce rather than reduce the body's stress response (Waltman et al 1993). As a matter of fact, several studies demonstrate that alcohol actually induces the stress response by stimulating hormone release by the hypothalamus, pituitary, and adrenal glands (Krishnan et al 1991;Tsigos and Chrousos 2002;Wand and Dobs 1991).…”

Section: Introductionmentioning

confidence: 99%

Chronic psychosocial stress causes delayed extinction and exacerbates reinstatement of ethanol-induced conditioned place preference in mice

Bahí

Dreyer

2013

Psychopharmacology

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Rationale We have shown previously, using an animal model of voluntary ethanol intake and ethanol-conditioned place preference (EtOH-CPP), that exposure to chronic psychosocial stress induces increased ethanol intake and EtOH-CPP acquisition in mice. Objective Here, we examined the impact of chronic subordinate colony (CSC) exposure on EtOH-CPP extinction, as well as ethanol-induced reinstatement of CPP. Methods Mice were conditioned with saline or 1.5 g/kg ethanol and were tested in the EtOH-CPP model. In the first experiment, the mice were subjected to 19 days of chronic stress, and EtOH-CPP extinction was assessed during seven daily trials without ethanol injection. In the second experiment and after the EtOH-CPP test, the mice were subjected to 7 days of extinction trials before the 19 days of chronic stress. Druginduced EtOH-CPP reinstatement was induced by a priming injection of 0.5 g/kg ethanol. Results Compared to the single-housed colony mice, CSC mice exhibited increased anxiety-like behavior in the elevated plus maze (EPM) and the open field tests. Interestingly, the CSC mice showed delayed EtOH-CPP extinction. More importantly, CSC mice showed increased alcohol-induced reinstatement of the EtOH-CPP behavior. Conclusion Taken together, this study indicates that chronic psychosocial stress can have long-term effects on EtOH-CPP extinction as well as drug-induced reinstatement behavior and may provide a suitable model to study the latent effects of chronic psychosocial stress on extinction and relapse to drug abuse.

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Free-choice ethanol consumption by rats: effects of ACTH4–10

Cited by 23 publications

References 23 publications

Effects of stress on alcohol drinking: a review of animal studies

Effects of stress on alcohol drinking: a review of animal studies

Alcohol: A stimulant activating brain stress responsive systems with persistent neuroadaptation

Chronic psychosocial stress causes delayed extinction and exacerbates reinstatement of ethanol-induced conditioned place preference in mice

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