Schedule-Induced Self-Administration of Drugs

Gilbert, R. M.

doi:10.1007/978-1-4613-3967-0_6

Cited by 11 publications

(5 citation statements)

References 88 publications

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“…In sweet solution binge drinking, the current practice is to add sweeteners to ethanol, a procedure long been used to promote ethanol drinking by rats. This animal model, originally termed sucrose fading, has face validity for the human condition because humans tend to initiate their drinking of alcohol in sweetened forms 103,104 . This is especially true early in the development of alcohol abuse/alcohol dependence, when consumption patterns reflect the NIAAA definition of binge drinking 2 .…”

Section: Preclinical Models Of Binge Drinkingmentioning

confidence: 99%

“…This animal model, originally termed sucrose fading, has face validity for the human condition because humans tend to initiate their drinking of alcohol in sweetened forms. 103,104 This is especially true early in the development of alcohol abuse/alcohol dependence, when consumption patterns reflect the NIAAA definition of binge drinking. 2 Adding sucrose or saccharin to sweeten ethanol solutions increases consumption by adult rats relative to ethanol alone in water [105][106][107][108] and sweeteners (at specific concentrations) alone in water.…”

Section: Sweet Solution ("Supersac") Binge Drinkingmentioning

confidence: 99%

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Preclinical studies of alcohol binge drinking

Crabbe

Harris

Koob

2011

Annals of the New York Academy of Sciences

185

159

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Binge drinking is prevalent and has serious biomedical consequences. In children, adolescents, and young adults, it is a prominent risk factor for later development of alcohol-use disorders. Many preclinical models have been employed to study the genetic risks for and biomedical consequences of alcohol drinking. However, these models historically did not result in bloodalcohol concentrations (BACs) exceding 80 mg%; this relatively modest level is the threshold that currently defines a binge session, according to the NIAAA and CDC. Nevertheless, in alcoholdependent rodents, binge drinking has been well documented. Key neurobiological substrates localized to brain reward and stress systems have been identified. Studies of newer models of binge drinking without dependence are reviewed here. In these models, rodents, non-human primates, and flies will drink enough to reach high BACs. They often display observable signs of intoxication. The neurobiological consequences of these episodes of binge drinking without dependence are reviewed, preliminary evidence for roles for GABA, glutamate, opioid peptides, and corticotropin releasing factor are discussed, as is the need for more work to identify the antecedents and consequences of binge drinking in both animal models and humans.

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Section: Preclinical Models Of Binge Drinkingmentioning

confidence: 99%

Section: Sweet Solution ("Supersac") Binge Drinkingmentioning

confidence: 99%

Preclinical studies of alcohol binge drinking

Crabbe

Harris

Koob

2011

Annals of the New York Academy of Sciences

185

159

View full text Add to dashboard Cite

show abstract

“…This animal model, unlike many others, contains construct validity for the human condition because humans tend to drink alcohol in a sweetened form (Gilbert, 1978;Samson et al, 1996), especially early in the development of alcohol abuse/ alcohol dependence when consumption patterns are reflective of the NIAAA definition of binge drinking (NIAAA, 2004). The addition of sweeteners (usually sucrose or saccharin) to the ethanol solution produces increase in consumption by adult rats relative to ethanol alone in water (Samson, 1986;Rassnick et al, 1992;Doremus et al, 2005;Truxell et al, 2007) and sweeteners (at specific concentrations) alone in water (Samson et al, 1996).…”

Section: Introductionmentioning

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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“…While in the chamber, subjects were continuously exposed to a polydipsia induction schedule (Falk, Samson, & Winger, 1972;Gilbert, 1978) in which, during every 4th h, a food pellet was delivered every 2 min. These pellets constituted the entire daily food ration.…”

Section: Methodsmentioning

confidence: 99%