Suppression of ethanol consumption by MET-enkephalin in rats

Ho, Andrew K.S.; Rossi, Nello

doi:10.1111/j.2042-7158.1982.tb04199.x

Cited by 48 publications

(9 citation statements)

References 3 publications

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“…The permanent nature of this finding may become significant in view of the fact that cerebrospinal fluid-injected condensation amine by-products of alcohol induce long-term alcohol consumption in rodents (19). There is animal evidence with regard to peptidyl opiate involvement in mediating alcohol-seeking behavior (16); and furthermore, it has been reported that human addicts have one-third the level of f-endorphin and significantly more adrenocorticotropic hormone in their cerebrospinal fluid than do normal volunteers (20). The results of this investigation indicate that the enkephalins may act as critical determinants for volitional consumption of ethanol (21).…”

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confidence: 64%

“…In addition, ethanol consumption is increased after opiate withdrawal (13). With the characterization of multiple opioid receptors (14) and stereospecific interactions of ethanol (15) and condensation byproducts (2) at 8 receptors, it is reasonable to suspect that some endogenous opioids may alter ethanol consumption in a way similar to opiates (16). Furthermore, it has been proposed (17) that ethanol-seeking behavior is genetically linked to a deficiency of the endogenous peptidyl opiates.…”

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confidence: 99%

“…From previous studies (16) volumes were recorded, and the animals were returned to food and water ad lib for 8 wk to minimize the effects of alcohol consumption. The animals then were decapitated, and their brains were removed (excluding the pituitary) and frozen on a dry block of dry ice.…”

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Ethanol acceptance as a function of genotype amounts of brain [Met]enkephalin.

Blum¹,

Elston²,

DeLallo³

et al. 1983

Proc. Natl. Acad. Sci. U.S.A.

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Our results indicate a negative correlation between the amount of ethanol (10%) consumed and endogenous levels of brain [Metlenkephalin in and DBA/2J (alcohol-nonpreferring) inbred mice strains. Additionally, it was found that 8 wk after 1-day starved groups of both C57BL/6J and DBA/2J mice were challenged with ethanol (10%) for 1-day acceptance, they had significantly lower levels of brain [Metlenkephalin compared with their nonalcohol-treated controls. These results suggest that the brain endogenous peptidyl opiates may play a crucial role in alcohol-seeldng behavior.Increasing evidence from both animals and man supports the interrelatedness between ethanol or condensation amine metabolites and opiates (1-5). Furthermore, there is support for the involvement of endogenous peptidyl opiates in the actions of ethanol (6-9). In this regard, experimental studies focused on the ability of the acute effects of opiate agonists to reduce the volitional consumption of ethanol in rats (10,11) MATERIAL AND METHODS Male C57BL/6J and DBA/2J mice (8 wk old) were obtained from The Jackson Laboratories, maintained at constant temperature (25 ± 2°C) and lighting (12 hr light/12 hr dark) conditions, and subsequently (14 wk old) tested for alcohol acceptance. -Baseline tap water drinking was established in both strains from day-to-day monitoring for 1 wk. Then they were separated into a control water-drinking group and an ethanolacceptance group. Control animals in both C57BL/6J and DBA/ 2J were matched with the experimental groups for the amount of water drinking. On the morning of day 8, fluid and food were removed from all groups for 24 hr. Then a 10% ethanol/tap water solution and tap water were administered to the treated group and control groups, respectively, for 24 hr. At 24 hr, their fluid volumes were recorded, and the animals were returned to food and water ad lib for 8 wk to minimize the effects of alcohol consumption. The animals then were decapitated, and their brains were removed (excluding the pituitary) and frozen on a dry block of dry ice. The samples were weighed and homogenized at 950C in a solution of 2 M acetic acid and then were heated for 5 min at 95TC. The samples then were chilled to 40C for 5 min and centrifuged at 14,000 x g for 15 min. The supernatant fractions were removed, shell-frozen in borosilicate tubes, and lyphilized overnight. The next day the residue was resuspended in 0.1 M phosphate buffer, pH 6.8/0.1% bovine serum albumin and centrifuged at 1,000 x g for 15 min. The supernatant fractions were then assayed for [Met]enkephalin (Immuno Nuclear kit, Stillwater MN). Duplicate samples were run, and a log/logit y/1 -y graph was used to determine binding. In order to insure dependability of the Immuno Nuclear enkephalin kit and our procedure, a series of validation tests were accomplished. Tocorroborate the immunological specificity, Boehringer Mannheim's [Met]enkephalin was compared with the enkephalin supplied with the kit. The effect of freezing versus nonfreezing was determined b...

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confidence: 64%

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confidence: 99%

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Ethanol acceptance as a function of genotype amounts of brain [Met]enkephalin.

Blum¹,

Elston²,

DeLallo³

et al. 1983

Proc. Natl. Acad. Sci. U.S.A.

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“…Although the role of opioid receptor systems in regulating the anxiolytic properties of ethanol has received less attention, there is evidence that this system mediates some of the motivational responses associated with ethanol administration (Wilson et al, 2003;Moller et al, 1997). Both high doses of morphine (Volpicelli et al, 1991) and intraventricular infusion of met-enkephalin (Ho and Rossi, 1982) decrease ethanol consumption in rats. Further, naltrexone (NAL) decreases operant responding for ethanol in rats, and decreases ethanol intake in rodents and humans (O'Malley et al, 2000;Hyytia and Sinclair, 1993;Froehlich et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

Microinjection of Naltrexone into the Central, but not the Basolateral, Amygdala Blocks the Anxiolytic Effects of Diazepam in the Plus Maze

Burghardt

Wilson

2005

Neuropsychopharmacol

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The amygdala is involved in behavioral and physiological responses to fear, and the anxiolytic properties of several drugs are localized to this region. Activation of endogenous opioid systems is known to occur in response to stress and a growing body of literature suggests that opioid systems regulate the properties of anxiolytic drugs. These experiments sought to elucidate the role of opioid receptors in the central (CeA) and basolateral (BLA) nuclei of the amygdala in regulating the anxiolytic properties of ethanol and diazepam. Male rats fitted with cannula received bilateral microinjections of the nonselective opioid receptor antagonist naltrexone (NAL) immediately followed by systemic delivery of either ethanol (1 g/kg) or diazepam (2 mg/kg) in the elevated plus maze. Both diazepam and ethanol decreased anxiety-like behavior. Delivery of NAL into the CeA blocked the anxiolytic properties of diazepam. Delivery of NAL into the BLA slightly increased open arm avoidance, but had no effect on the anxiolytic properties of diazepam. Microinjection of NAL into either nucleus failed to block the effects of ethanol. These results were specific to the anxiolytic properties of diazepam, since baseline behaviors were unaffected by microinjection of NAL. Microinjection of lidocaine produced results distinct from NAL and failed to block the anxiolytic actions of diazepam. These studies indicate distinct roles for opioid receptor systems in the CeA and BLA in regulating the anxiolytic properties of diazepam in the elevated plus maze. Further, opioid receptor systems in the CeA and BLA do not regulate the anxiolytic properties of ethanol in this test.

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“…The suppression also occurs under conditions in which conditioned taste aversions could not form (Sinclair et al, 1974b(Sinclair et al, , 1982. A suppression is also produced by methadone , by levorphanol but not dextrophan Ross, 1976), and by met-enkephalin (Ho & Rossi, 1981;Ho, 1982), with the latter effect and that by morphine being blocked by naloxone (Ho, 1982). In contrast to the suppression with moderate or high doses of opiates, low doses can increase alcohol drinking by rats (Beaman et al, 1984;Reid & Hunter, 1984), with very low doses (0.005 and 0.025 mg/kg) of diprenorphine producing greater increases than a larger dose (0.05 mg/kg) (Hunter et al, 1984).…”

Section: Opiatesmentioning

confidence: 99%

The Feasibility of Effective Psychopharmacological Treatments for Alcoholism

Sinclair

1987

British Journal of Addiction

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The effects of lithium, anxiolytics, dopaminergic compounds, serotonin uptake inhibitors, opiates, opiate antagonists, and alcohol-sensitizing drugs on the alcohol consumption of human alcoholics and laboratory animals are reviewed. There is increasing evidence that each of these classes of drugs might be beneficial in reducing alcohol abuse, including recent controlled studies on alcoholics with lithium, serotonin uptake blockers, and disulfiram. The usefulness of all ofthe current drugs, however, appears limited, and the ideal drug for use in treating alcoholism awaits discovery. Nevertheless, the fact that some drugs acting on the central nervous system are able to promote abstinence supports the feasibility of psychopharmacological treatment for alcoholism. Furthermore, since the known drugs that appear beneficial against human alcohol abuse also suppress voluntary alcohol selection by experimental animals, it seems likely that studies with animals could be used for screening other potentially effective drugs. dehyde, and liver aldehyde dehydrogenase relationships. Effects of ethyleneglycol dinitrate and related compounds on ethanol preference and ethanol metabolism, Acta Pharmacologica et Toxicologica, 35, pp. 145-154.

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Suppression of ethanol consumption by MET-enkephalin in rats

Cited by 48 publications

References 3 publications

Ethanol acceptance as a function of genotype amounts of brain [Met]enkephalin.

Ethanol acceptance as a function of genotype amounts of brain [Met]enkephalin.

Microinjection of Naltrexone into the Central, but not the Basolateral, Amygdala Blocks the Anxiolytic Effects of Diazepam in the Plus Maze

The Feasibility of Effective Psychopharmacological Treatments for Alcoholism

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