Naloxone decreases ethanol consumption within a free choice paradigm in rats

Sandi, Carmen; Borrell, José; Guaza, Carmen

doi:10.1016/0091-3057(88)90270-5

Cited by 39 publications

(6 citation statements)

References 25 publications

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“…In the case of naloxone, many animal studies have demonstrated a suppression of ethanol intake in rats treated with this drug (Myers and Critcher 1982;Sandi et al 1988;Froehlich et al 1990;Davidson and Amit 1996). However, naloxone is also found to suppress intake of palatable foodstuffs (Apfelbaum and Mandenoff 1981;Schwarz-Stevens et al 1992;Cleary et al 1996), raising doubt about the specificity of the alcohol effect (Herz 1997).…”

Section: Discussionmentioning

confidence: 94%

The motivation for beer in rats: effects of ritanserin, naloxone and SR 141716

Gallate¹,

McGregor²

1999

Psychopharmacology

184

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Rats were given two weeks of home cage access to either "near-beer" (a beverage that tastes like beer but contains <0.5% ethanol v/v) or near-beer with added ethanol (4.5% v/v), which is simply referred to as "beer". The two groups of rats (near-beer and beer) were then trained on a "lick-based progressive ratio paradigm" in operant chambers in which an ever increasing number of licks had to be emitted for each successive fixed unit of near-beer or beer delivered. Break points (the ratio at which responding ceased) for near-beer and beer were approximately equal under baseline conditions. Rats were then tested for the effects of the 5HT2A/2C receptor antagonist ritanserin (0.625, 2.5 or 10 mg/kg), the opioid receptor antagonist naloxone (0.625, 2.5 or 10 mg/kg) or the cannabinoid CB1 receptor antagonist SR 141716 (0.3, 1 or 3 mg/kg). All three drugs caused a dose-dependent reduction of break-points and locomotor activity in both the beer and near-beer groups. However, the effects of SR 141716 and naloxone, but not ritanserin, on breakpoints were significantly more pronounced on rats drinking beer compared to those drinking near-beer. There were no such differential effects of any of the drugs on locomotor activity across the two groups. These results suggest that both SR 141716 and naloxone differentially affect the motivation to consume alcoholic beverages and may thus have potential as drugs for the treatment of alcohol craving.

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Section: Discussionmentioning

confidence: 94%

The motivation for beer in rats: effects of ritanserin, naloxone and SR 141716

Gallate¹,

McGregor²

1999

Psychopharmacology

184

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“…Animal studies have shown that the administration of naloxone and naltrexone decreases ethanol self-administration (see Ulm et al, 1995 for a review). This antagonist-induced decrease in ethanol intake has been observed in a wide variety of settings including home-cage drinking (Marfaing-Jallat et al, 1983;Reid and Hunter, 1984;Hubbell et al, 1986;Sandi et al, 1988;Froehlich et al, 1990) and operant paradigms (Samson and Doyle, 1985;Weiss et al, 1990;Hyytia and Sinclair, 1993;June et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Effects of Naltrexone Alone and In Combination With Acamprosate on the Alcohol Deprivation Effect in Rats

Heyser

Moc

Koob

2003

Neuropsychopharmacol

101

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Previous research in our laboratory has shown that responding for ethanol increases after a period of imposed deprivation during which no ethanol is available (the alcohol deprivation effect). This selective increase in responding for ethanol was blocked by chronic administration of acamprosate. In the present study the effects of naltrexone and the combination of naltrexone+acamprosate on oral ethanol self-administration were examined following an imposed period of abstinence. Male Wistar rats were trained to respond for ethanol (10% w/v) or water in a two-lever free-choice condition. After training, separate groups of rats received chronic injections (2 Â /day) of saline, naltrexone, or naltrexone+acamprosate during a 5-day period of abstinence. Ethanol self-administration was tested in all groups of rats on the last day of abstinence, 30 min after the last drug injection. Responding for ethanol increased significantly following the deprivation period in animals treated with saline. Chronic administration of naltrexone and the combination naltrexone+acamprosate blocked the increased ethanol consumption following the imposed abstinence period on post-deprivation Day 1. On post-deprivation Day 2, the combination of acamprosate with naltrexone blocked the rebound increase in ethanol consumption observed in animals treated with a low dose of naltrexone. These results support the hypothesis that naltrexone and acamprosate are effective in modulating aspects of alcohol-seeking behavior, and under certain situations may be more effective in combination.

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“…Naltrexone decreases ethanol consumption in humans , rodents (Reid et al, 1997), and monkeys (Kornet et al 1992), an effect that does not diminish with time (Reid et al, 1997), whereas morphine at high doses decreases and at low doses increases ethanol consumption (Hubbel et al, 1993). Stresses that release endogenous opiates decrease ethanol consumption whereas the poststress increase in drinking can be blocked by naloxone (Sandi et al, 1988). Although many effects of ethanol cannot be explained on the basis of opiate action (e.g., naloxone does not induce signs of withdrawal in animals physically dependent on ethanol and ethanol does not competitively displace naloxone from the opiate receptor), the evidence suggests some link between the -receptor and ethanol.…”

Section: Discussionmentioning

confidence: 99%