Buprenorphine alters ethanol self-administration in rats: dose-response and time-dependent effects

June, Harry L.; Cason, Charity R; Chen, Shen-Hsing Annabel; Lewis, Michael J.

doi:10.1007/s002130050735

Cited by 12 publications

(10 citation statements)

References 35 publications

(66 reference statements)

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“…The present finding that the partial opiate agonist buprenorphine produced a dose-dependent decrease in heroin intake in heroindependent rats is consistent with previous findings in opiate-dependent nonhuman primates (Mello et al, 1983;Winger et al, 1992) and humans (Mello and Mendelson, 1980;Comer et al, 2001Comer et al, , 2002, and as such provide some predictive validity for the current model. Interestingly, the doses selected for buprenorphine in the present study were effective in reducing the self-administration of other drugs of abuse in rats (Martin et al, 1983;Myers et al, 1984;Carroll and Lac, 1992;June et al, 1998). All low doses selected for naloxone were effective in increasing drug intake in heroin-dependent rats, similar in part to a previous study (Carrera et al, 1999).…”

Section: Discussionsupporting

confidence: 82%

“…Rats were injected with buprenorphine (0, 0.01, 0.04, and 0.2 mg/kg, s.c.) for four consecutive days (days 49-52) using a within-subjects Latin-square design 15 min prior to the active phase (1800-0600 h). Doses were selected based on work from previous investigators (Martin et al, 1983;Myers et al, 1984;Carroll and Lac, 1992;June et al, 1998) and preliminary trials of the present study.…”

Section: Buprenorphine Challengementioning

confidence: 99%

See 1 more Smart Citation

Unlimited Access to Heroin Self-Administration: Independent Motivational Markers of Opiate Dependence

Chen

O’Dell

Hoefer

et al. 2006

Neuropsychopharmacol

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The goal of the present study was to develop and validate an animal model of unlimited access to intravenous heroin self-administration combined with responding for food and water to characterize the transition to drug dependence. Male Wistar rats were allowed to lever press for heroin (60 mg/kg/0.1 ml infusion/s; fixed ratio 1; 20-s time out) and nosepoke for food and water in consecutive, daily 23-h sessions. Daily heroin intake increased over days, reaching significance by Day 14. Drug-taking increased across the circadian cycle, reflected as increases in both the nocturnal peak and diurnal nadir of heroin intake. Changes in the circadian pattern of food intake and meal patterning preceded and paralleled the changes in heroin intake. By Day 7, the circadian amplitude of feeding was blunted. Nocturnal intake decreased because rats consumed smaller and briefer meals. Diurnal intake increased due to increased meal frequency, whereas total daily food intake decreased. To control for time or experience in the self-administration boxes as a possible confound, rats with saline (no drug) tethers were tested and did not display significant changes in food intake pattern. Body weight gain slowed slightly in heroin rats relative to saline controls. Separate groups of rats revealed that significant physical dependence as measured by physical signs of opiate withdrawal following a naloxone injection (1.0 mg/kg, subcutaneous (s.c.)) was reached by Day 14. Significant increases in heroin intake could be produced using low doses of naloxone (0.003-0.03 mg/kg, s.c.) on days 28-31 of heroin access. After 6 weeks of heroin self-administration, rats injected with buprenorphine (0, 0.01, 0.04, and 0.2 mg/kg, s.c.) showed a dose-dependent reduction in heroin intake. Changes in the pattern of drug and food intake in the present unlimited heroin access model may serve as independent motivational markers for the transition to a drug-dependent state.

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Section: Discussionsupporting

confidence: 82%

Section: Buprenorphine Challengementioning

confidence: 99%

Unlimited Access to Heroin Self-Administration: Independent Motivational Markers of Opiate Dependence

Chen

O’Dell

Hoefer

et al. 2006

Neuropsychopharmacol

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“…As far as additional consumption of ethanol is concerned, our results (9% sublingual buprenorphine; 17% methadone) are in contrast to the findings of June et al [77] and Musshoff, Lachenmeier & Madea [78] who found a consumption rate of 40%. In order to determine whether buprenorphine has the capacity to attenuate the reinforcing effects of ethanol, June et al [77] conducted a systematic examination of both dose-and time-dependent effects of buprenorphine on ethanol intake in rats trained to selfadministration ethanol using an ascending concentration procedure.…”

Section: Discussioncontrasting

confidence: 83%

Maintenance Treatment of Opioid Dependence and Patterns of Non-Prescribed Drug Use: Results of a 4-Year Trial

Giacomuzzi¹,

Ertl²,

Pavlic³

et al. 2006

LDDD

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To establish the extent to which participants in maintenance treatment programmes (methadone and sublingual buprenorphine) used opioids, benzodiazepines, ethanol, cocaine and amphetamines, and to define the pattern of such use over time.Design: A retrospective analysis of data of 42,610 analyses from urinalysis screening.Setting: Outpatient drug treatment centre, Measurements: Enzyme-multiplied immunoassay and gas chromatography-mass spectrometry.Results: Urine samples from 23.4% (N = 4998) of those in the methadone treatment group and 16.5% (N = 1110) in the sublingual buprenorphine group tested positive for consumption of additional drugs (p < 0.001). The most frequently detected drugs were benzodiazepines (63% of all methadone, and 40% of all sublingual buprenorphine positive samples; (p < 0.001)) and opioids (26% of all methadone, and 21% of all sublingual buprenorphine positive samples; (p < 0.001)). In both of the treatment programmes morphine abuse (63%) was higher than heroin (7%). There was a significant decrease of benzodiazepine abuse in the study period (2000)(2001)(2002)(2003) both among clients receiving methadone (p < 0.001) and those receiving sublingual buprenorphine (p = 0.006). Benzodiazepine (Spearman rank correlation coefficient r = 0.281, p < 0.001), cocaine (r = 0.057, p = 0.007), ethanol (r = 0.073, p= 0.028) and morphine (r = -0.179, p < 0.001) abuse were associated with age in sublingual buprenorphine treated patients. Methadone clients showed a lifetime relation for cocaine (r = -0.032, p = 0.007), ethanol (Spearman corr. coeff. r = 0.118, p < 0.001), morphine (r = -0.107, p < 0.001) and dihydrocodeine abuse (r = 0.093, p < 0.001). Discussion:The present data indicate that nonprescribed drug use remains a persistent problem for patients in maintenance treatment. Substances misused are mainly opioids and benzodiazepines. Non-prescribed morphine has replaced heroin.

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“…Although it is not approved for the treatment of cocaine or alcohol abuse, buprenorphine has been shown to decrease the self-administration of both of those drugs as well in rodents, non-human primates, and people (Martin et al, 1983;Mello et al, 1989;June et al, 1998). However, the exact mechanism of this action is not known.…”

Section: Abbreviationsmentioning

confidence: 99%

Nociceptin/Orphanin FQ Receptor Activation Attenuates Antinociception Induced by Mixed Nociceptin/Orphanin FQ/μ-Opioid Receptor Agonists

Khroyan

Polgar²,

Jiang³

et al. 2009

J Pharmacol Exp Ther

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Activation of brain nociceptin/orphanin FQ (NOP) receptors leads to attenuation of -opioid receptor (MOP receptor)-mediated antinociception. Buprenorphine, a high-affinity partial MOP receptor agonist also binds to NOP receptors with 80 nM affinity. The buprenorphine-induced inverted U-shaped doseresponse curve for antinociception may be due to NOP receptor activation, given that, in the presence of the NOP receptor antagonist, 1-[(3R,4R)-1-cyclooctylmethyl-3-hydroxymethyl-4-piperidyl]-3-ethyl-1,3-dihydro-2H-benzimidazol-2-one (J113397), or in NOP receptor knockout mice, buprenorphine has a steeper dose-response curve and acts as a full agonist. To further explore the involvement of the direct activation of NOP receptors by buprenorphine and other compounds that activate both NOP and MOP receptors, the antinociceptive effects of 1-(1-(2,3,3␣,4,5,6-hexahydro-1H-phenalen-1-yl)piperidin-4-yl)-indolin-2-one. (SR16435), 3-ethyl-1-(1-(4-isopropylcyclohexyl)piperidin-4-yl)-indolin-2-one (SR16507), buprenorphine, pentazocine, and morphine, compounds with varying levels of MOP and NOP receptor affinity and efficacy, were assessed in mice using the tail-flick assay. The ability of the selective NOP receptor antagonist (Ϫ)-cis-1-methyl-7-[[4-(2,6-dichlorophenyl)piperidin-1-yl]methyl]-6,7,8,9-tetrahydro-5H-benzocyclohepten-5-ol (SB-612111) to potentiate antinociception induced by the above compounds was examined to investigate whether activation of NOP receptors leads to attenuation of MOP receptormediated antinociception. SB-612111 potentiated antinociception induced by buprenorphine and the other mixed NOP/MOP receptor agonists SR16435 and SR16507. However, SB-612111 had no effect on pentazocine or morphine antinociception, two compounds with no NOP receptor-binding affinity. These results further support the hypothesis that activation of NOP receptors can lead to attenuation of MOP receptormediated antinociception elicited by mixed NOP/MOP receptor compounds such as buprenorphine, SR16435, and SR16507 and that, although buprenorphine has low efficacy in vitro, it has significant NOP receptor agonist activity in vivo.

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Buprenorphine alters ethanol self-administration in rats: dose-response and time-dependent effects

Cited by 12 publications

References 35 publications

Unlimited Access to Heroin Self-Administration: Independent Motivational Markers of Opiate Dependence

Unlimited Access to Heroin Self-Administration: Independent Motivational Markers of Opiate Dependence

Maintenance Treatment of Opioid Dependence and Patterns of Non-Prescribed Drug Use: Results of a 4-Year Trial

Nociceptin/Orphanin FQ Receptor Activation Attenuates Antinociception Induced by Mixed Nociceptin/Orphanin FQ/μ-Opioid Receptor Agonists

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