Morphine and naloxone modulate intake of ethanol

Reid, Larry D.; Hunter, George A.

doi:10.1016/0741-8329(84)90033-8

Cited by 192 publications

(62 citation statements)

References 14 publications

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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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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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“…Therefore, an important step in the development of new treatments for AUDs is to identify receptors and/or neural pathways that are altered by ethanol consumption during development. A large body of evidence suggests the MOP-R plays a role in ethanol-mediated behaviors (Reid and Hunter, 1984;Gardell et al, 1996;Stromberg et al, 1998;Lê et al, 1999;Roberts et al, 2000;Hall et al, 2001;Becker et al, 2002;Ciccocioppo et al, 2002). Similarly, the DOP-R is dynamically regulated by ethanol exposure (Charness et al, 1993;Winkler et al, 1998;Méndez et al, 2004), is implicated in ethanol reward (Froehlich et al, 1991;Borg and Taylor, 1997;Froehlich et al, 1998;Matsuzawa et al, 1999a,b;Shippenberg et al, 2008), and plays a role in ethanol self-administration.…”

Section: Introductionmentioning

confidence: 99%

δ-Opioid Receptor Function in the Dorsal Striatum Plays a Role in High Levels of Ethanol Consumption in Rats

Nielsen¹,

Simms²,

Li³

et al. 2012

J. Neurosci.

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Binge-like patterns of excessive drinking during young adulthood increase the propensity for alcohol use disorders (AUDs) later in adult life; however, the mechanisms that drive this are not completely understood. Previous studies showed that the ␦-opioid peptide receptor (DOP-R) is dynamically regulated by exposure to ethanol and that the DOP-R plays a role in ethanol-mediated behaviors. The aim of this study was to determine the role of the DOP-R in high ethanol consumption from young adulthood through to late adulthood by measuring DOP-R-mediated [ 35 S]GTP␥S binding in brain membranes and DOP-R-mediated analgesia using a rat model of high ethanol consumption in Long Evans rats. We show that DOP-R activity in the dorsal striatum and DOP-R-mediated analgesia changes during development, being highest during early adulthood and reduced in late adulthood. Intermittent access to ethanol but not continuous ethanol or water from young adulthood leads to an increase in DOP-R activity in the dorsal striatum and DOP-R-mediated analgesia into late adulthood. Multiple microinfusions of naltrindole into the dorsal striatum or multiple systemic administration of naltrindole reduces ethanol consumption, and following termination of treatment, DOP-R activity in the dorsal striatum is attenuated. These findings suggest that DOP-R activity in the dorsal striatum plays a role in high levels of ethanol consumption and suggest that targeting the DOP-R is an alternative strategy for the treatment of AUDs.

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“…One such antagonist, naltrexone, has been shown in numerous single center and multicenter placebo‐controlled clinical trials to improve treatment outcomes for alcoholics by decreasing relapse (Anton et al., 1999; Guardia et al., 2002; Heinala et al., 2001; Latt, Jurd, Houseman, & Wutzke, 2002; Oslin, Liberto, O'Brien, Krois, & Norbeck, 1997; Volpicelli, Alterman, Hayashida, & O'Brien, 1992), craving (Chick et al., 2000; Heinala et al., 2001; Volpicelli et al., 1992), days of drinking (Monti et al., 2001; O'Malley et al., 1992; Volpicelli et al., 1992) and number of drinks if the patient drank during treatment (Anton et al., 1999; Chick et al., 2000; Monti et al., 2001). Consistent with these clinical findings, there have also been reports from preclinical studies in laboratory animals that describe naltrexone‐induced decreases in ethanol intake (Froehlich, Harts, Lumeng, & Li, 1987, 1990; Hubbell et al., 1986; Myers & Lankford, 1996; Parkes & Sinclair, 2000; Phillips, Wenger, & Dorow, 1997; Reid & Hunter, 1984), ethanol self‐administration (Heyser, Roberts, Schulteis, & Koob, 1999; Samson & Doyle, 1985; Sinden, Marfaing‐Jallat, & Le Magnen, 1983; Williams, Kane, & Woods, 2001), and the expression of ethanol‐induced conditioned place preference (Bechtholt & Cunningham, 2005; Cunningham, Henderson, & Bormann, 1998; Kuzmin, Sandin, Terenius, & Ogren, 2003; Middaugh & Bandy, 2000). Nevertheless, naltrexone is not always effective in humans (Gastpar et al., 2002; Kranzler, Modesto‐Lowe, & Van Kirk, 2000; Krystal, Cramer, Krol, Kirk, & Rosenheck, 2001).…”

Section: Introductionmentioning

confidence: 99%

Kappa‐opioid receptors differentially regulate low and high levels of ethanol intake in female mice

et al. 2016

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IntroductionStudies in laboratory animals and humans indicate that endogenous opioids play an important role in regulating the rewarding value of various drugs, including ethanol (EtOH). Indeed, opioid antagonists are currently a front‐line treatment for alcoholism in humans. Although roles for mu‐ and delta‐opioid receptors have been characterized, the contribution of kappa‐opioid receptors (KORs) is less clear. There is evidence that changes in KOR system function can decrease or increase EtOH drinking, depending on test conditions. For example, female mice lacking preprodynorphin – the precursor to the endogenous KOR ligand dynorphin – have reduced EtOH intake. Considering that KORs can regulate dopamine (DA) transmission, we hypothesized that KORs expressed on DA neurons would play a prominent role in EtOH intake in females.MethodsWe used a Cre/loxP recombination strategy to ablate KORs throughout the body or specifically on dopamine uptake transporter (DAT)‐expressing neurons to investigate the role of KORs on preference for and intake of EtOH (2‐bottle choice), the transition from moderate to excessive EtOH drinking (intermittent EtOH access), and binge EtOH drinking (drinking in the dark [DID]).Results KOR deletion decreased preference for EtOH, although this effect was less pronounced when EtOH intake increased beyond relatively low levels.DiscussionOur findings indicate that KOR activation increases EtOH drinking via effects mediated, at least in part, by KORs on DA neurons. While the mechanisms of this regulation remain unknown, previous work suggests that alterations in negative reinforcement processes or sensitivity to the sensory properties of EtOH can affect preference and intake.

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Morphine and naloxone modulate intake of ethanol

Cited by 192 publications

References 14 publications

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

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

δ-Opioid Receptor Function in the Dorsal Striatum Plays a Role in High Levels of Ethanol Consumption in Rats

Kappa‐opioid receptors differentially regulate low and high levels of ethanol intake in female mice

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