Consumption of ethanol solution is potentiated by morphine and attenuated by naloxone persistently across repeated daily administrations

Hubbell, Christopher L.; Czirr, Stephanie A.; Hunter, George A.; Beaman, Carol M.; LeCann, Noelle C.; Reid, Larry D.

doi:10.1016/0741-8329(86)90070-4

Cited by 215 publications

(77 citation statements)

References 50 publications

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“…These results confirm previous reports that opioid receptor antagonists reduce ethanol intake (Samson and Doyle, 1985;Hubbell et al, 1986;Froehlich et al, 1990;Weiss et al, 1990;Hyytia and Sinclair, 1993;June et al, 1999) and attenuate the ethanol deprivation effect (Hölter and Spanagel, 1999;Hölter et al, 2000). The reduction in responding for ethanol below baseline observed after administration of the higher doses (0.125 and 0.25 mg/kg) of naltrexone was specific to the first day after ethanol deprivation.…”

Section: Discussionsupporting

confidence: 81%

“…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%

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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: Discussionsupporting

confidence: 81%

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

View full text Add to dashboard Cite

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“…Pharmacological studies indicate that opioid receptor antagonists, such as naloxone hydrochloride and naltrexone, decrease alcohol self-administration in animal models (Altshuler et al 1980;Froehlich et al 1990;Hubbell et al 1986Hubbell et al , 1991Marfaing-Jallat et al 1983;Samson and Doyle 1985;Weiss et al 1990). Clinical trials demonstrated that naltrexone reduces alcohol drinking and self-reported "high," alcohol craving, as well as relapse rates in recently abstinent outpatient alcohol-dependent patients (O'Malley et al 1992;Volpicelli et al 1992Volpicelli et al , 1995 .…”

mentioning

confidence: 99%

Naltrexone Dampens Ethanol-Induced Cardiovascular and Hypothalamic- Pituitary-Adrenal Axis Activation

McCaul

2001

Neuropsychopharmacology

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Alcohol ingestion activates the autonomic nervous system and the hypothalamic-pituitary-adrenal axis. This study examined naltrexone effects on alcohol-induced increases in physiological responses and their association with alcohol liking. Using a within-subjects design, heavy drinking men (N ϭ 19) were maintained on each of three naltrexone doses (0, 50, and 100 mg, p.o.) over an 8-day inpatient stay. Within each naltrexone dose, subjects had three alcohol challenge sessions (none, moderate, high) The brain opioid system has been proposed to be part of the neurocircuitry involved in alcohol reward and heavy alcohol drinking (Froehlich and Wand 1997;Gianoulakis and deWaele 1994;Reid et al. 1991). Pharmacological studies indicate that opioid receptor antagonists, such as naloxone hydrochloride and naltrexone, decrease alcohol self-administration in animal models (Altshuler et al. 1980;Froehlich et al. 1990;Hubbell et al. 1986Hubbell et al. , 1991Marfaing-Jallat et al. 1983;Samson and Doyle 1985;Weiss et al. 1990). Clinical trials demonstrated that naltrexone reduces alcohol drinking and self-reported "high," alcohol craving, as well as relapse rates in recently abstinent outpatient alcohol-dependent patients (O'Malley et al. 1992;Volpicelli et al. 1992Volpicelli et al. , 1995 . These findings led to naltrexone's approval by the Food and Drug Administration as a pharmacotherapeutic agent for the treatment of alcohol dependence. Naltrexone is thought to reduce alcohol-induced high and relapse by binding to opioid receptors in discrete brain regions associated with reward and craving, and to prevent receptor activation by alcohol-induced release of endogenous opioid peptides.Alcohol induces a variety of acute physiological responses when consumed in moderate-to-high doses. It is well established that intoxicating doses of alcohol increase heart rate (Docter et al. 1966;Iwase et al. 1995 McCaul et al. 1989;Sellers et al. 1972;Turkkan et al. 1988;van de Borne et al. 1997). These heart rate increases are hypothesized to be positively associated with the reinforcing or appetitive motivational effects of alcohol (Peterson et al. 1996) . Alcohol has less predictable effects on blood pressure, with reports of blood pressure increases (Iwase et al. 1995;Sellers et al. 1972) and no effects following alcohol ingestion (Turkkan et al. 1988;van de Borne et al. 1997). Finally, alcoholinduced peripheral vasodilation and associated skin temperature increases have been consistently reported (Iwase et al. 1995;Turkkan et al. 1988) and is thought to be one explanation for the lack of a consistent rise in blood pressure after alcohol consumption.Acute administration of intoxicating doses of alcohol also activates the hypothalamic-pituitary-adrenal (HPA) axis thereby increasing ACTH and glucocorticoid levels (Inder et al. 1995;Rivier et al. 1984;Waltman et al. 1993). It remains unclear whether alcohol-induced activation of the HPA axis has any relationship to its reinforcing properties. Rodent studies show that alcohol increases pla...

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“…For example, animal studies have demonstrated slowed acquisition of alcohol self-administration (Phillips et al 1997) and decreased alcohol consumption following administration of the non-selective opioid receptor antagonists naloxone (Froehlich et al 1990;Hubbell et al 1986;Hyytia and Sinclair 1993 ;Reid et al 1991;Weiss et al 1990), naltrexone (Altshuler et al 1980Boyle et al 1998;Davidson and Amit 1997 ;Myers et al 1986;Reid et al 1996;Volpicelli et al 1986), and nalmefene . The second line of evidence for functional involvement of the opioid system in mediating alcohol drinking behavior comes from neurobiological studies which indicate that alcohol alters opioid peptide systems.…”

mentioning

confidence: 99%

Naltrexone Alters Subjective and Psychomotor Responses to Alcohol in Heavy Drinking Subjects

McCaul

Wand

Eissenberg

et al. 2000

Neuropsychopharmacology

110

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(Czirr et al. 1987;Hubbell et al. 1986;Reid et al. 1991). For example, animal studies have demonstrated slowed acquisition of alcohol self-administration (Phillips et al. 1997) and decreased alcohol consumption following administration of the non-selective opioid receptor antagonists naloxone (Froehlich et al. 1990;Hubbell et al. 1986;Hyytia and Sinclair 1993 ;Reid et al. 1991;Weiss et al. 1990), naltrexone (Altshuler et al. 1980Boyle et al. 1998;Davidson and Amit 1997 ;Myers et al. 1986;Reid et al. 1996;Volpicelli et al. 1986), and nalmefene . The second line of evidence for functional involvement of the opioid system in mediating alcohol drinking behavior comes from neurobiological studies which indicate that alcohol alters opioid peptide systems. Acute alcohol administration increases endorphin and enkephalin gene expression in discrete brain regions of rodents, increases opioid peptide release from both brain and pituitary of

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Consumption of ethanol solution is potentiated by morphine and attenuated by naloxone persistently across repeated daily administrations

Cited by 215 publications

References 50 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

Naltrexone Dampens Ethanol-Induced Cardiovascular and Hypothalamic- Pituitary-Adrenal Axis Activation

Naltrexone Alters Subjective and Psychomotor Responses to Alcohol in Heavy Drinking Subjects

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