Increasing the rate of ethanol consumption in food- and water-satiated rats

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

“…Adding sweeteners to ethanol solutions to produce higher ethanol intake is not a new experimental strategy. Some of the disadvantages of earlier procedures are, however, circumvented in the present model, such as the need for food deprivation (e.g., Macdonall and Marcucella, 1979) or water deprivation (e.g., Hubbell et al, 1986;Reid et al, 1996;Gardell et al, 1997), or the lack of a defined BAL criterion (e.g., Stewart and Grupp, 1984;Gill et al, 1986;Linseman, 1987;Sinclair et al, 1992). Although genetic manipulations have been used to produce animals that reliably and voluntarily consume large quantities of ethanol (e.g., HARF animals, Lê et al, 2001;P rats, Murphy et al, 1986), selective breeding is not a practical solution for most laboratories.…”

“…Collectively, these models have weak construct validity for the human condition (i.e., humans do not consume ethanol because they are hungry or thirsty). Other studies have produced voluntary ethanol consumption by rats during limited access sessions without the use of any of these manipulations but those studies either did not produce BALs (0.08 g%) determined by NIAAA to be the defining factor in binge alcohol drinking (e.g., Stewart and Grupp, 1984;Gill et al, 1986;Linseman, 1987) or did not measure BALs (e.g., Macdonall and Marcucella, 1979). Finally, genetic manipulations have been used to produce rats selectively bred for high alcohol preference based on either continuous access ethanol intakes (e.g., alcohol-preferring P rats; Murphy et al, 1986) or limited access ethanol intakes (i.e., high alcohol-consuming HARF rats; Lê et al, 2001).…”

“…Gilpin and G.F. Koob, unpublished findings), produce significant neurobiological perturbations that are likely associated with dependence-induced drinking. Other models of binge-like alcohol self-administration have employed water deprivation (e.g., Hubbell et al, 1986;Reid et al, 1996;Gardell et al, 1997) or food deprivation (e.g., MacDonall and Marcucella, 1979;Falk and Tang, 1988) to promote ethanol self-administration during daily limited-access periods. These designs are problematic, however, because animals are primarily motivated by thirst during self-administration sessions and body weight gain is slowed or completely blocked with such procedures.…”

The Genetic Complexity of Alcohol Drinking in Rodents

“…In general, restricted access does increase intakes Gill, France, & Amit, 1986;Grahame & Grose, 2003;Le, Ko, Chow, & Quan, 1994;MacDonall & Marcucella, 1979;Marcucella & Munro, 1987), and such paradigms can yield animals that show signs of intoxication (Cronise, Finn, Metten, & Crabbe, 2005). In general, restricted access does increase intakes Gill, France, & Amit, 1986;Grahame & Grose, 2003;Le, Ko, Chow, & Quan, 1994;MacDonall & Marcucella, 1979;Marcucella & Munro, 1987), and such paradigms can yield animals that show signs of intoxication (Cronise, Finn, Metten, & Crabbe, 2005).…”

“…In general, restricted access does increase intakes Gill, France, & Amit, 1986;Grahame & Grose, 2003;Le, Ko, Chow, & Quan, 1994;MacDonall & Marcucella, 1979;Marcucella & Munro, 1987), and such paradigms can yield animals that show signs of intoxication (Cronise, Finn, Metten, & Crabbe, 2005). Limited access to alcohol rather than restricted availability of food and water seems to be sufficient to elevate intakes over repeated daily sessions (MacDonall & Marcucella, 1979;Marcucella & Munro, 1987). This model initially restricts and then gradually relaxes access to fluids until a point is reached at which the effects of fluid limitation per se are assumed to be minimized.…”