Periodic availability: Factors affecting alcohol selection in rats

Holloway, Frank; Bird, David C.; Devenport, J.A.

doi:10.1016/0741-8329(84)90031-4

Cited by 21 publications

(15 citation statements)

References 19 publications

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“…Although the BALs found in this study are far below those typical of most tolerance and dependence studies in rats, they compare favourably with those obtained in other drinking studies (Kulkosky 1980;Holloway et al 1984;Stewart and Grupp 1984;Grant and Samson 1985), even though the latter involved sweetening of the alcohol solutions, higher concentrations of alcohol, or food deprivation. In the past investigators have interpreted only gross signs of intoxication in rats as evidence that pharmacologically significant amounts of alcohol were being consumed.…”

Section: Discussionsupporting

confidence: 54%

Alcohol consumption in free-feeding rats: procedural, genetic and pharmacokinetic factors

Linseman¹

1987

Psychopharmacology

115

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Voluntary consumption of alcohol by rats (i.e. in the absence of food or water deprivation, sweetening of the alcohol solution, etc.) that results in the attainment of behaviorally significant or pharmacologically detectable blood alcohol levels (BALs) has been difficult to demonstrate. In this study, we showed that free-feeding Wistar rats given access to increasingly concentrated solutions of alcohol in separate "drinking" cages on a 1-h per day basis drank on average close to 1 g/kg, resulting in average BALs close to 50 mg%. This drinking was comparable to that obtained by rats trained according to a procedure used widely by others in which animals are maintained at reduced body weights. Weight restriction alone, however, did not enhance amount of alcohol consumption over that of free-feeding animals in the 1-h session. There was also a strain difference in that Wistar rats drank significantly more than did Sprague-Dawley rats. Post hoc absorption curves showed that the initial absorption of alcohol from both the stomach and the peritoneum was slower in Wistar than in Sprague-Dawley rats, suggesting rate of absorption may be inversely related to amount of alcohol consumed; metabolic rates and volumes of distribution appeared unrelated to consumption. This periodic availability paradigm might be useful to investigate the effect of biological variables on individual bouts of alcohol consumption.

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Section: Discussionsupporting

confidence: 54%

Alcohol consumption in free-feeding rats: procedural, genetic and pharmacokinetic factors

Linseman¹

1987

Psychopharmacology

115

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“…The current paradigm of intermittent access to ethanol (i.e. 2 days a week with varying lengths of deprivation between access periods) was chosen as a valid animal model of alcoholism, as intermittent access: (1) tends to produce greater ethanol consumption in rodents than continuous 24 h access paradigms (Pinel & Huang, 1976; Holloway et al . 1984; Linseman, 1987; Samson, 1987); (2) is more characteristic of ‘binge’ pattern drinking seen in human alcoholics (Mendelson & Mello, 1966; Epstein et al .…”

Section: Discussionmentioning

confidence: 99%

Reduced operant ethanol self‐administration and in vivo mesolimbic dopamine responses to ethanol inPKCε‐deficient mice

Olive

Mehmert

Messing

et al. 2000

Eur J of Neuroscience

125

103

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There is increasing evidence that individual protein kinase C (PKC) isozymes mediate specific effects of ethanol on the nervous system. In addition, multiple lines of evidence suggest that the mesoaccumbens dopamine reward system is critically involved in the rewarding and reinforcing effects of ethanol. Yet little is known about the role of individual PKC isozymes in ethanol reinforcement processes or in regulation of mesolimbic systems. In this study, we report that mice lacking the epsilon isoform of PKC (PKCepsilon) show reduced operant ethanol self-administration and an absence of ethanol-induced increase in extracellular dopamine levels in the nucleus accumbens. PKCepsilon null mice exhibited a 53% decrease in alcohol-reinforced operant responses under basal conditions, as well as following ethanol deprivation. Behavioural analysis revealed that while both genotypes had the same number of drinking bouts following deprivation, PKCepsilon null mice demonstrated a 61% reduction in number of ethanol reinforcers per bout and a 57% reduction in ethanol-reinforced response rate. In vivo microdialysis experiments showed that, in contrast to wild-type mice, PKCepsilon null mice exhibited no change in extracellular levels of dopamine in the nucleus accumbens following acute administration of ethanol (1 and 2 g/kg i.p.), while mesolimbic dopamine responses to cocaine (20 mg/kg i.p.) or high potassium (100 mM) in these mice were comparable with that of wild-types. These data provide further evidence that increases in extracellular mesolimbic dopamine levels contribute to the reinforcing effects of ethanol, and indicate that pharmacological agents inhibiting PKCepsilon may be useful in the treatment of alcohol dependence.

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“…In order to get a rodent to consume sufficient amounts of ethanol, experimental manipulations are required. These experimental/environmental manipulations include fluid deprivation (Sandi et al, 1990), schedule-induced polydipsia (Ford, 2014; Meisch, 1975, 2001), scheduled availability (Holloway et al, 1984) including intermittent every-other-day access (Carnicella et al, 2014), sucrose-fading (Samson, 1986), and/or forced induction of dependence (Deutsch and Eisner, 1977); which can be achieved intragastrically (Crews, 2008; French, 2001), intraperitoneally (Pascual et al, 2009, 2014), by ethanol-vapor exposure (Roberts et al, 2000; Vendruscolo and Roberts, 2014), chronic drinking of a liquid ethanol diet (Brown et al, 2004; Lieber and DeCarli, 1989), or long-term drinking with water and food concurrently available (Vengeliene et al, 2009). Most of these methods include an integral stress factor, which does have some face validity with the clinical condition (Al’Absi, 2007).…”

Section: Background From An Animal Model Perspectivementioning

confidence: 99%

Rat animal models for screening medications to treat alcohol use disorders

et al. 2017

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The purpose of this review is to present animal research models that can be used to screen and/or repurpose medications for the treatment of alcohol abuse and dependence. The focus will be on rats and in particular selectively bred rats. Brief introductions discuss various aspects of the clinical picture, which provide characteristics of individuals with alcohol use disorders (AUDs) to model in animals. Following this, multiple selectively bred rat lines will be described and evaluated in the context of animal models used to screen medications to treat AUDs. Next, common behavioral tests for drug efficacy will be discussed particularly as they relate to stages in the addiction cycle. Tables highlighting studies that have tested the effects of compounds using the respective techniques are included. Wherever possible the Tables are organized chronologically in ascending order to describe changes in the focus of research on AUDs over time. In general, high ethanol-consuming selectively bred rats have been used to test a wide range of compounds. Older studies usually followed neurobiological findings in the selected lines that supported an association with a propensity for high ethanol intake. Most of these tests evaluated the compound's effects on the maintenance of ethanol drinking. Very few compounds have been tested during ethanol-seeking and/or relapse and fewer still have assessed their effects during the acquisition of AUDs. Overall, while a substantial number of neurotransmitter and neuromodulatory system targets have been assessed; the roles of sex- and age-of-animal, as well as the acquisition of AUDs, ethanol-seeking and relapse continue to be factors and behaviors needing further study.

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Periodic availability: Factors affecting alcohol selection in rats

Cited by 21 publications

References 19 publications

Alcohol consumption in free-feeding rats: procedural, genetic and pharmacokinetic factors

Alcohol consumption in free-feeding rats: procedural, genetic and pharmacokinetic factors

Reduced operant ethanol self‐administration and in vivo mesolimbic dopamine responses to ethanol inPKCε‐deficient mice

Rat animal models for screening medications to treat alcohol use disorders

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