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

Zhou, Yan; Kreek, Mary Jeanne

doi:10.1016/j.neuropharm.2014.05.044

Cited by 33 publications

(23 citation statements)

References 150 publications

(163 reference statements)

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“…One of the critical factors influencing individual vulnerability to drug relapse is atypical stress responsivity [Kreek and Koob, 1998;Zhou and Kreek, 2014]. Using many validated experimental models, like the forced swim and elevated plus maze tests in rodents, anxiety-like and depression-like behaviors have been demonstrated after chronic alcohol, mostly during its acute withdrawal [Colombo et al, 2006;Bell et al, 2012;Becker and Happel, 2012].…”

Section: V1b Receptor and Arginine Vasopressin (Avp) Systemmentioning

confidence: 99%

Involvement of Activated Brain Stress Responsive Systems in Excessive and “Relapse” Alcohol Drinking in Rodent Models: Implications for Therapeutics

Zhou

Kreek

2018

J Pharmacol Exp Ther

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Addiction to specific drugs (such as alcohol, psychostimulants and opioids) shares some common direct or downstream effects on the brain stress-responsive systems, including arginine vasopressin and its V1b receptors, dynorphin and the kappa opioid receptors, proopiomelanocortin/β-endorphin and the mu opioid receptors, and the endocannabinoids. Further study of these systems, through laboratory-based and translational research, could lead to the discovery of novel treatment targets and the early optimization of interventions (for example, combination) for the pharmacological therapy of alcoholism.

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Section: V1b Receptor and Arginine Vasopressin (Avp) Systemmentioning

confidence: 99%

Involvement of Activated Brain Stress Responsive Systems in Excessive and “Relapse” Alcohol Drinking in Rodent Models: Implications for Therapeutics

Zhou

Kreek

2018

J Pharmacol Exp Ther

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“…Preclinical investigations have consistently found that NTN decreases alcohol intake and alcohol’s reinforcing and motivational properties [Zhou and Kreek 2014]. In select experiments, therefore, we used the well-known MOP-r antagonist NTN as a reference compound to compare its effects on mouse alcohol drinking behaviors with those of the KOP-r agonist MSB.…”

Section: Introductionmentioning

confidence: 99%

Synergistic blockade of alcohol escalation drinking in mice by a combination of novel kappa opioid receptor agonist Mesyl Salvinorin B and naltrexone

et al. 2017

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Mesyl Salvinorin B (MSB) is a potent selective kappa opioid receptor (KOP-r) agonist that has potential for development as an anti-psychostimulant agent with fewer side-effects (e.g., sedation, depression and dysphoria) than classic KOP-r agonists. However, no such study has been done on alcohol. We investigated whether MSB alone or in combination with naltrexone (mu-opioid receptor antagonist) altered voluntary alcohol drinking in both male and female mice. Mice, subjected to 3 weeks of chronic escalation drinking (CED) in a two-bottle choice paradigm with 24-h access every other day, developed rapid escalation of alcohol intake and high preference. We found that single, acute administration of MSB dose-dependently reduced alcohol intake and preference in mice after 3-week CED. The effect was specific to alcohol, as shown by the lack of any effect of MSB on sucrose or saccharin intake. We also used the drinking-in-the-dark (DID) model with limited access (4 h/day) to evaluate the pharmacological effect of MSB after 3 weeks of DID. However, MSB had no effect on alcohol drinking after 3-week DID. Upon investigation of potential synergistic effects between naltrexone and MSB, we found that acute administration of a combination of MSB and naltrexone reduced alcohol intake profoundly after 3-week CED at doses lower than those individual effective doses. Repeated administrations of this combination showed less tolerance development than repeated MSB alone. Our study suggests that the novel KOP-r agonist MSB both alone and in combination with naltrexone shows potential in alcoholism treatment models.

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“…Together, these results clearly demonstrate that the URB597-induced inhibition of FAAH plays a role in modulating alcohol drinking in mice. Therefore, the development of FAAH inhibitors with improved pharmacokinetics has the potential to yield useful compounds for the treatment of alcoholism and other drug addictions [Panlilio et al 2013; Zhou & Kreek 2014]. …”

Section: Discussionmentioning

confidence: 99%

Blockade of alcohol escalation and “relapse” drinking by pharmacological FAAH inhibition in male and female C57BL/6J mice

et al. 2017

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Background Anandamide (AEA)-dependent signaling is regulated by the catabolic enzyme fatty acid amide hydrolase (FAAH). Several lines of evidence have demonstrated that FAAH and AEA are involved in the behavioral effects of alcohol. Therefore, we investigated whether a selective FAAH inhibitor, URB597 (Cyclohexylcarbamic acid 3′-[aminocarbonyl]-[1,1′-biphenyl]-3-yl ester), altered alcohol intake in mice in a voluntary alcohol drinking model. Methods Mice, subjected to 3 weeks of chronic intermittent access (IA) in a two-bottle choice paradigm with 24-h access every other day, developed rapid escalation of alcohol intake and high preference. We evaluated the pharmacological effects of URB597 after both acute (1-day) withdrawal from chronic IA and 1-week withdrawal using the alcohol deprivation effect (ADE) model. AEA and N-acyl ethanolamide (NAE) abundances were determined after chronic IA, acute (1-day) or long-term (1 and 2 weeks) withdrawal in four brain regions. Results Acute pretreatment with URB597 reduced alcohol intake and preference after acute withdrawal. This effect was blocked by pretreatment with a selective type 1 cannabinoid receptor (CB1) antagonist, suggesting a CB1-mediated mechanism. Both single- and multiple- dosing regimens with an effective dose of URB597 prevented the ADE, with no tolerance development after the multi-dosing regimen. AEA and NAE levels were transiently increased in all brain regions measured after acute withdrawal, indicating that the endocannabinoid system is involved in acute alcohol withdrawal stress response. Conclusion FAAH inhibitors reduce alcohol escalation and “relapse” drinking in mice.

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

Cited by 33 publications

References 150 publications

Involvement of Activated Brain Stress Responsive Systems in Excessive and “Relapse” Alcohol Drinking in Rodent Models: Implications for Therapeutics

Involvement of Activated Brain Stress Responsive Systems in Excessive and “Relapse” Alcohol Drinking in Rodent Models: Implications for Therapeutics

Synergistic blockade of alcohol escalation drinking in mice by a combination of novel kappa opioid receptor agonist Mesyl Salvinorin B and naltrexone

Blockade of alcohol escalation and “relapse” drinking by pharmacological FAAH inhibition in male and female C57BL/6J mice

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