A new factor affecting the consumption of ethyl alcohol and other sapid fluids

Wayner, M.J.; Greenberg, Isaac; Tartaglione, R.; Nolley, D.; Fraley, S.; Cott, Anne C. Van

doi:10.1016/0031-9384(72)90383-6

Cited by 106 publications

(36 citation statements)

References 10 publications

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“…Specifically, the deprivation effect, a temporary increase in a particular reward-seeking behavior seen after absence of the reward, can illuminate relapse-like behavior. A saccharin deprivation effect (SDE) is seen in rats, with increasing magnitude as length of deprivation increases, suggesting that deprivation effect is a general reward phenomenon, not involved with withdrawal, or simply relegated to drugs of abuse (Neznanova et al, 2002;Wayner et al, 1972;Sinclair and Senter, 1968). …”

Section: Introductionmentioning

confidence: 99%

Effects of alcohol and saccharin deprivations on concurrent ethanol and saccharin operant self-administration by alcohol-preferring (P) rats

Toalston

Oster

Kuc

et al. 2008

Alcohol

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Consumption of sweet solutions has been associated with a reduction in withdrawal symptoms and alcohol craving in humans. The objective of the present study was to determine the effects of EtOH and saccharin (SACC) deprivations on operant oral self-administration. P rats were allowed to lever press concurrently self-administer EtOH (15% v/v) and SACC (0.0125% g/v) for 8 weeks. Rats were then maintained on daily operant access (non-deprived), deprived of both fluids (2 weeks), deprived of SACC and given 2 ml of EtOH daily, or deprived of EtOH and given 2 ml of SACC daily. All groups were then given two weeks of daily operant access to EtOH and SACC, followed by an identical second deprivation period. P rats responded more for EtOH than SACC. All deprived groups increased responding on the EtOH lever, but not on the SACC lever. Daily consumption of 2 ml EtOH decreased the duration of the ADE. Home cage access to 2 ml SACC also decreased the ADE but to a lesser extent than access to EtOH. A second deprivation period further increased and prolonged the expression of an ADE. These results show EtOH is a more salient reinforcer than SACC. With concurrent access to EtOH and SACC, P rats do not display a saccharin deprivation effect. Depriving P rats of both EtOH and SACC had the most pronounced effect on the magnitude and duration of the ADE, suggesting that there may be some interactions between EtOH and SACC in their CNS reinforcing effects.

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Section: Introductionmentioning

confidence: 99%

Effects of alcohol and saccharin deprivations on concurrent ethanol and saccharin operant self-administration by alcohol-preferring (P) rats

Toalston

Oster

Kuc

et al. 2008

Alcohol

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“…Although this may be difficult to achieve on an absolute level, it is possible to equate operant responding for a saccharin solution with that observed for ethanol. This may be particularly relevant given that a type of deprivation effect is also observed with saccharin solution (Wayner et al 1972), although the patten of responding is different than that observed in animals deprived of ethanol (Sinclair et al 1973). Therefore, although it does appear that acamprosate affects ethanol intake, additional tests need to be conducted to examine the effects of acamprosate on other reinforcers.…”

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confidence: 99%

Chronic Acamprosate Eliminates the Alcohol Deprivation Effect While Having Limited Effects on Baseline Responding for Ethanol in Rats

Heyser

Schulteis

Durbin³

et al. 1998

Neuropsychopharmacology

168

112

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“…Alternating sessions of access with sessions of nonaccess augments the effect (Amit, Stern, & Wise, 1970;Pinel & Huang, 1976;Veale & Myers, 1969;Wayner & Greenberg, 1972;Wayner, Greenberg, Carey, & Nolley, 1971;Wise, 1973). For example, reported increased ethanol consumption following a restricted-access schedule wherein ethanol was presented for 2 days and withheld for 2 days.…”

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confidence: 99%

“…The failure of procedures to induce oral consumption of ethanol for its pharmacological effect (Lester, 1966;Mardones, 1960;Meisch, 1977;Mello, 1973;Myers & Veale, 1972;Wallgren & Barry, 1970;Wayner & Greenberg, 1972) hasbeen attributed to either the aversive taste of ethanol (Altshuler, Weaver, & Phillips, 1975;Mello, 1973) or to the delay between ingestion and the onset of its pharmacological effect (Lester & Freed, 1973;Mello, 1973). Yet failure to consume because of taste and delay Presented at the Seventh Harvard Symposium on Quantitative Analyses of Behavior: Biological Determinants, Harvard University, June [8][9]1984.…”

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confidence: 99%

Predicting the amount of ethanol consumed per bout from schedule of access to ethanol

Marcucella

1989

Animal Learning & Behavior

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The present paper suggests that the difficulty in inducing animals to orally self-administer quantities of ethanol sufficient to produce dependence is related to the schedule of ethanol access. If the variables that control the various patterns of ethanol consumption can be identified, then the patterns of ethanol consumption leading to excessive intake and the development of dependence will be able to be identified and generated experimentally. Evidence is presented which shows that the amount of ethanol consumed per bout, the daily frequency of ethanol bouts, as well as the total amount of ethanol consumed, is a function of the frequency of ethanol access periods, feeding condition, ethanol concentration, and the temporal proximity of ethanol access periods.In the attempt to discover the variables responsible for the development of human alcoholism, many investigators have attempted to induce excessive ethanol consumption in nonhuman organisms. Modeling pathology in animals has proved enormously useful in other areas of science and medicine, and there is little reason to believe, a priori, that an animal model of human alcoholism would not contribute to our understanding of human alcoholism. Not only could the many presumed psychological causes of alcoholism, such as stress, for example, be examined under controlled conditions, but also treatment techniques having the potential to decrease consumption could be designed andtested. An adequate animal model would also help determine the physiological effects of prolonged ethanol consumption uncontaminated by the possible nutritional and other health-eare deficiencies usually observed in human alcoholics.Unfortunately, nonhuman organisms do not spontaneously consume ethanol in amounts that readily lead to intoxication or the development of physical dependence. The failure of procedures to induce oral consumption of ethanol for its pharmacological effect (

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A new factor affecting the consumption of ethyl alcohol and other sapid fluids

Cited by 106 publications

References 10 publications

Effects of alcohol and saccharin deprivations on concurrent ethanol and saccharin operant self-administration by alcohol-preferring (P) rats

Effects of alcohol and saccharin deprivations on concurrent ethanol and saccharin operant self-administration by alcohol-preferring (P) rats

Chronic Acamprosate Eliminates the Alcohol Deprivation Effect While Having Limited Effects on Baseline Responding for Ethanol in Rats

Predicting the amount of ethanol consumed per bout from schedule of access to ethanol

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