Reestablishing an Intragastric Ethanol Self‐infusion Model in Rats

Fidler, Tara L.; Clews, Tara W.; Cunningham, Christopher L.

doi:10.1111/j.1530-0277.2006.00046.x

Cited by 36 publications

(57 citation statements)

References 32 publications

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“…In other words, and in accordance with recent studies conducted in adult rats (Fidler et al 2006;Kiefer et al 2005;Samson and Czachowski 2003), it appears that acceptance of ethanol requires a balance between the sensory and postabsorptive effects of the drug. Unpublished preliminary data indicate that blood ethanol levels (BELs) achieved at the end of conditioning on PD 16 resulted in approximately 20 mg/dl.…”

Section: Discussionsupporting

confidence: 84%

Naloxone attenuation of ethanol-reinforced operant responding in infant rats in a re-exposure paradigm

et al. 2011

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Self-administration of ethanol was established in terms of operant responding in preweanling rats with no previous exposure to the drug. Pairing of naloxone with ethanol, at a point separate in time from operant responding, reduced ethanol reinforcement. This indicated participation of the opioid system in ethanol reinforcement. This effect seems not to be unique to ethanol but also is observable when sucrose acts as reinforcer.

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Section: Discussionsupporting

confidence: 84%

Naloxone attenuation of ethanol-reinforced operant responding in infant rats in a re-exposure paradigm

et al. 2011

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“…Passive IG ethanol infusion is one of the most effective and rapid ways of producing physical dependence (Fidler et al, 2006). In comparison, chronic intermittent ethanol vapors may take a few cycles of exposure to induce dependence (Finn et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Differential effects of ghrelin antagonists on alcohol drinking and reinforcement in mouse and rat models of alcohol dependence

et al. 2015

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An effort has been mounted to understand the mechanisms of alcohol dependence in a way that may allow for greater efficacy in treatment. It has long been suggested that drugs of abuse seize fundamental reward pathways and disrupt homeostasis to produce compulsive drug seeking behaviors. Ghrelin, an endogenous hormone that affects hunger state and release of growth hormone, has been shown to increased alcohol intake following administration, while antagonists decrease intake. Using rodent models of dependence, the current study examined the effects of two ghrelin receptor antagonists, [DLys3]-GHRP-6 (DLys) and JMV2959, on dependence-induced alcohol self-administration. In two experiments adult male C57BL/6J mice and Wistar rats were made dependent via intermittent ethanol vapor exposure. In another experiment, adult male C57BL/6J mice were made dependent using the intragastric alcohol consumption (IGAC) procedure. Ghrelin receptor antagonists were given prior to voluntary ethanol drinking. Ghrelin antagonists reduced ethanol intake, preference, and operant self-administration of ethanol and sucrose across these models, but did not decrease food consumption in mice. In experiments 1 and 2, voluntary drinking was reduced by ghrelin receptor antagonists, however this reduction did not persist across days. Despite the transient effects to ghrelin antagonists, the drugs had renewed effectiveness following a break in administration as seen in experiment 1. The results show the ghrelin system as a potential target for studies of alcohol abuse. Further research is needed to determine the central mechanisms of these drugs and their influence on addiction in order to design effective pharmacotherapies.

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“…Binge alcohol exposure procedures that utilize forced alcohol administration that is either passive (e.g. repeated experimenter-administered intragastric alcohol infusions; Crews et al, 2000;Crews and Braun, 2003) or active (e.g., bout drinking via consumption of alcohol liquid diet as the sole source of nutrition; Fidler et al, 2006; N.W. Gilpin and G.F. Koob, unpublished findings), produce significant neurobiological perturbations that are likely associated with dependence-induced drinking.…”

Section: Discussionmentioning

confidence: 99%

Effects of naltrexone, duloxetine, and a corticotropin-releasing factor type 1 receptor antagonist on binge-like alcohol drinking in rats

Gilpin²,

Richardson³

et al. 2008

Behavioural Pharmacology

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A 'binge' is defined by National Institute on Alcohol Abuse and Alcoholism as an excessive pattern of alcohol drinking that produces blood-alcohol levels (BALs) greater than 0.08 g% within a 2-h period and may or may not be associated with dependence. The purpose of this investigation was to explore the effects of several neuropharmacological agents in an animal model in which outbred rats voluntarily and orally self-administer pharmacologically meaningful alcohol doses that produce BALs ≥ 0.08 g% in daily limited access two-bottle choice and operant drinking sessions. Rats were trained to self-administer either 10% (w/v) alcohol solution sweetened with 'supersac' (3% glucose + 0.125% saccharin) or supersac alone versus water in a two-bottle choice or operant situation during 30-min daily sessions. Rats were then injected systemically with multiple doses of duloxetine, naltrexone, and the corticotropin-releasing factor antagonist, MPZP, in Latin-square designs. Alcohol binge drinkers reliably consumed amounts of alcohol sufficient to produce BALs ≥ 0.08 g%. Duloxetine dose-dependently suppressed two-bottle choice alcohol binge drinking and operant alcohol responding as well as operant supersac responding, but did not affect two-bottle choice supersac drinking. Naltrexone-suppressed alcohol binge drinking at very low doses and suppressed supersac drinking at moderate-to-high doses. MPZP did not affect alcohol or supersac consumption. Different profiles for drugs that suppress binge-like alcohol drinking compared with dependenceinduced drinking provide a heuristic foundation for future medications development.

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Reestablishing an Intragastric Ethanol Self‐infusion Model in Rats

Cited by 36 publications

References 32 publications

Naloxone attenuation of ethanol-reinforced operant responding in infant rats in a re-exposure paradigm

Naloxone attenuation of ethanol-reinforced operant responding in infant rats in a re-exposure paradigm

Differential effects of ghrelin antagonists on alcohol drinking and reinforcement in mouse and rat models of alcohol dependence

Effects of naltrexone, duloxetine, and a corticotropin-releasing factor type 1 receptor antagonist on binge-like alcohol drinking in rats

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