OPIOIDS <406>
Database EMBASE
Accession Number 2005177716
Authors De Wet C.J. Reed L.J. Bearn J.
Institution
(De Wet, Reed, Bearn) Wickham Park House, South London and Maudsley NHS Trust, Bethlem Royal Hospital,
Beckenham, Kent, United Kingdom.
(Reed, Bearn) Natl. Addict. Ctr. Inst. Psychiat., London, United Kingdom.
(Bearn) Wickham Park House, South London and Maudsley NHS Trust, Bethlem Royal Hospital, Monks Orchard
Road, Beckenham Kent BR3 3BX, United Kingdom.
Country of Publication
United Kingdom
Title
The rise of buprenorphine prescribing in England: Analysis of NHS regional data,
2001-03.
Source
Addiction. 100(4)(pp 495-499), 2005. Date of Publication: Apr 2005.
Abstract
Aims: Since its launch in the prescribing market in 1999 for the treatment of opiate
dependence, buprenorphine has rapidly become established as an alternative to methadone
treatment in the United Kingdom. In the absence of evidence of its clinical superiority over
methadone, and given its high relative cost, we sought to examine the impact of
buprenorphine availability on opiate treatment services in England. Methods: Quarterly
buprenorphine and methadone community prescription ligures were obtained for 28 Strategic
Health Authorities (SHAs) in England, for the 2-year period September 2001 to September
2003. Rates of buprenorphine prescribing (as proportion of all opiate prescriptions) were
examined over time by number of prescriptions and net ingredient cost. Results:
Buprenorphine prescription rates increased disproportionately to methadone in all 28 SHAs.
By the end of 2003 the number of buprenorphine prescriptions had increased to 23% of all
opiate prescriptions, but accounted for 45% of opiate prescription costs in England.
Buprenorphine prescribing rates varied substantially across different regions. Conclusions:
Buprenorphine prescribing has increased dramatically and represents a disproportionately
large fraction of community opiate prescribing costs. The marked regional variation suggests
the need for further research and the development of national guidelines to support rational
prescribing and equitable access to treatment. copyright 2005 Society for the Study of
Addiction.
ISSN 0965-2140
Publication Type Journal: Article
Journal Name Addiction
Volume 100
Issue Part 4
Page 495-499
Year of Publication 2005
Date of Publication Apr 2005
OPIOIDS <410>
Database
EMBASE
Accession Number
2005177712
Authors
Degenhardt L. Reuter P. Collins L. Hall W.
Institution
(Degenhardt, Collins, Hall) Natl. Drug and Alcohol Res. Centre, University of New South Wales, Sydney, NSW
2052, Australia.
(Reuter) School of Public Policy, Department of Criminology, University of Maryland, United States.
(Hall) Office of Public Policy and Ethics, Institute for Molecular Bioscience, University of Queensland, St Lucia, QLD,
Australia.
Country of Publication
United Kingdom
Title
Evaluating explanations of the Australian 'heroin shortage'.
Source
Addiction. 100(4)(pp 459-469), 2005. Date of Publication: Apr 2005.
Abstract
Aims: In this paper we outline and evaluate competing explanations for a heroin shortage
that occurred in Australia during 2001 with an abrupt onset at the beginning of 2001.
Methods: We evaluated each of the explanations offered for the shortage against evidence
from a variety of sources: government reports, police and drug law enforcement documents
and briefings, key informant (KI) interviews, indicator data and research data. Results: No
similar shortage occurred at the same time in other markets (e.g. Vancouver, Canada or
Hong Kong) whose heroin originated in the same countries as Australia's. The shortage was
due most probably to a combination of factors that operated synergistically and sequentially.
The heroin market had grown rapidly in the late 1990s, perhaps helped by a decline in drug
law enforcement (DLE) in Australia in the early 1990s that facilitated high-level heroin
suppliers in Asia to establish large-scale importation heroin networks into Australia. This led
to an increase in the availability of heroin, increasingly visible street-based drug markets,
increased purity and decreased price of heroin around the country. The Australian heroin
market was well established by the late 1990s, but it had a low profit margin with high heroin
purity, and a lower price than ever before. The surge in heroin problems led to increased
funding of the Australian Federal Police and Customs as part of the National Illicit Drug
Strategy in 1998-99, with the result that a number of key individuals and large seizures
occurred during 1999-2000, probably increasing the risks of large-scale importation. The
combination of low profits and increased success of law enforcement may have reduced the
dependability of key suppliers of heroin to Australia at a time when seized heroin was
becoming more difficult to replace because of reduced supplies in the Golden Triangle. These
factors may have reduced the attractiveness of Australia as a destination for heroin trafficking.
Conclusions: The Australian heroin shortage in 2001 was due probably to a combination of
factors that included increased effectiveness of law enforcement efforts to disrupt networks
bringing large shipments of heroin from traditional source countries, and decreased capacity
or willingness of major traffickers to continue large scale shipments to Australia. copyright
2005 Society for the Study of Addiction.
ISSN 0965-2140
Publication Type Journal: Review
Journal Name Addiction
Volume 100
Issue Part 4
Page 459-469
Year of Publication 2005
Date of Publication Apr 2005
OPIOIDS (A) <425>
Database EMBASE
Accession Number 2005172106
Authors Skoubis P.D. Lam H.A. Shoblock J. Narayanan S. Maidment N.T.
Institution
(Skoubis, Lam, Shoblock, Narayanan, Maidment) Dept. of Psychiat./Biobehav. Sci., Neuropsychiatric Institute, Univ.
of California at Los Angeles, Los Angeles, CA 90024, United States.
(Skoubis) Neuroscience Research, Global Pharmaceut. Res. and Devmt., Abbott Laboratories, 100 Abbott Park
Road, Abbott Park, IL 60064, United States.
(Narayanan) Glenmark Pharmaceuticals Ltd., Glenmark Research Centre, MIDC, T.T.C. Industrial Area, Navi
Mumbai 400 709, India.
Country of Publication
United Kingdom
Title
Endogenous enkephalins, not endorphins, modulate basal hedonic state in mice.
Source
European Journal of Neuroscience. 21(5)(pp 1379-1384), 2005. Date of Publication: Mar
2005.
Abstract
The aversive response to naloxone administration observed in human and animal studies
suggests the presence of an endogenous opioid tone regulating hedonic state but the
class(es) of opioid peptides mediating such opioid hedonic tone is uncertain. We sought to
address this question using mice deficient in either beta-endorphin or pro-enkephalin in a
naloxone-conditioned place aversion paradigm. Mice received saline in the morning in one
chamber and either saline or naloxone (0.1, 1 or 10 mg/kg, s.c.) in the afternoon in another
chamber, each day for 3 days. On the test day they were given free access to the testing
chambers in the afternoon and the time spent in each chamber was recorded. Whereas wildtype and beta-endorphin-deficient mice exhibited a robust conditioned place aversion to
naloxone, pro-enkephalin knockout mice failed to show aversion to naloxone at any dose
tested. In contrast, these mice showed a normal conditioned aversion to the kappa opioid
receptor agonist, 1150,488 (5 mg/kg), and to LiCl (100 mg/kg) indicating that these mice are
capable of associative learning. In a separate experiment, pro-enkephalin knockout mice,
similar to wild-type and beta-endorphin-deficient mice, demonstrated a significant conditioned
place preference to morphine (2.5, 5 and 10 mg/kg s.c.). These data suggest that
enkephalins, but not endorphins, may mediate an endogenous opioid component of basal
affective state and also indicate that release of neither endogenous enkephalins nor
endorphins is critical for the acquisition or expression of the association between contextual
cues and the rewarding effect of exogenously administered opiates.
ISSN 0953-816X
Publication Type Journal: Article
Journal Name European Journal of Neuroscience
Volume 21
Issue Part 5
Page 1379-1384
Year of Publication 2005
Date of Publication Mar 2005
OPIOIDS <438>
Database
EMBASE
Accession Number
2005145216
Authors
Gu J. Yao M. Wang J. Zhou W. Yang G. Liu H. Zhang Z. Liu X.
Institution
(Gu, Yao, Wang, Zhang, Liu) Inst. of Biochem. and Cell Biology, Shanghai Institutes for Biol. Sci., Chinese
Academy of Sciences, Shanghai 200031, China.
(Gu, Liu) Xinyuan Inst. of Med. and Biotech., School of Life Sciences, Zhejiang University of Sci.-Tech., Hangzhou
310018, China.
(Yao) Andrus Gerontology Center, University of Southern California, Los Angeles, CA 90089, United States.
(Zhou, Yang, Liu) Inst. Ningbo Addict. Res. Treatm., Ningbo 315010, China.
Country of Publication
United Kingdom
Title
Suppression of morphine withdrawal syndrome by interleukin-2 and its gene.
Source
NeuroReport. 16(4)(pp 387-391), 2005. Date of Publication: 15 Mar 2005.
Abstract
The naloxone-precipitated withdrawal syndrome in mice and rats after intrathecal injection of
recombinant human interleukin-2 protein (rIL-2) or its gene was studied. The results showed
that rIL-2 could significantly decrease the number of jumps in mice. In rats, rIL-2 significantly
suppressed irritating, diarrhea, weight loss, abnormal posture and salivation. Tendencies
towards reductions in teeth chewing and dog-shaking were also observed. Furthermore,
pcDNA3-IL-2 (8 mug DNA) had a similar effect as 1 x 10⁴ IU rIL-2 protein on
inhibition of morphine withdrawal syndrome in mice, and the expression of rIL-2 protein in
spinal cord could be detected for 6 days. These findings provided further evidence for the
neuroregulatory function of an immunological molecule such as IL-2. copyright 2005
Lippincott Williams & Wilkins.
ISSN 0959-4965
Publication Type Journal: Article
Journal Name NeuroReport
Volume 16
Issue Part 4
Page 387-391
Year of Publication 2005
Date of Publication 15 Mar 2005
OPIOIDS <439>
Database EMBASE
Accession Number 2005143487
Authors Gabra B.H. Afify E.A. Daabees T.T. Abou Zeit-Har M.S.
Institution
(Gabra) Inst. of Pharmacology of Sherbrooke, School of Medicine, University of Sherbrooke 3001, 12E Avenue
Nord, Sherbrooke, Que. J1H5N4, Canada.
(Afify, Daabees, Abou Zeit-Har) Department of Pharmacology, Faculty of Pharmacy, University of Alexandria,
Alexandria, Egypt.
Country of Publication
United Kingdom
Title
The role of the NO/NMDA pathways in the development of morphine withdrawal
induced by naloxone in vitro.
Source
Pharmacological Research. 51(4)(pp 319-327), 2005. Date of Publication: Apr 2005.
Abstract
The effect of nitric oxide (NO)/N-methyl-d-aspartate (NMDA) pathways on naloxone-induced
withdrawal contracture was studied in vitro in a model of acute morphine dependence in the
isolated guinea pig ileum. Exposure of the isolated guinea pig ileum to morphine (10⁵ M) for 5 min resulted in acute dependence, characterized by a strong withdrawal
contracture induced by naloxone (5 x 10^-5 M). The NO synthase (NOS) inhibitor
N ^G-nitro-l-arginine methyl ester (l-NAME; 5 x 10^-4 M) as well as
the soluble guanylate cyclase inhibitor methylene blue (MB; 10 muM) were found to
significantly attenuate the naloxone-induced withdrawal contracture. In addition, the NO
precursor l-arginine (5 x 10^-4 M) as well as the NO donors sodium nitroprusside
(SNP; 1 muM) and sodium azide (NaZ; 10 muM) were able to revert the effect of l-NAME
returning the amplitude of naloxone-induced contracture to the same level in control
morphine-dependent ilea. We also demonstrated that the competitive NMDA receptor
antagonist dl-2-amino-5-phosphonovaleric acid (AP-5; 50 muM) potently reduced the
amplitude of naloxone-induced contracture in the same model, an effect that was reversed by
co-administration of the excitatory amino acid l-glutamate (40 muM). This in vitro study
confirms the implication of the NO/NMDA pathways in morphine dependence. copyright 2004
Elsevier Ltd. All rights reserved.
ISSN 1043-6618
Publication Type Journal: Article
Journal Name Pharmacological Research
Volume 51
Issue Part 4
Page 319-327
Year of Publication 2005
Date of Publication Apr 2005
OPIOIDS (A) <465>
Database EMBASE
Accession Number 2005120481
Authors Grasing K. He S.
Institution
(Grasing, He) Substance Abuse Research Laboratory, Kansas City Vet. Aff. Medical Center, 4801 Linwood
Boulevard, Kansas City, MO, United States.
(Grasing) Division of Clinical Pharmacology, Department of Medicine, Univ. of Kansas School of Medicine, Kansas
City, MO, United States.
(Grasing) Research Service, 151, 4801 Linwood Boulevard, Kansas City, MO 64128, United States.
Country of Publication
United Kingdom
Title
Effects of high-dose selegiline on morphine reinforcement and precipitated
withdrawal in dependent rats.
Source
Behavioural Pharmacology. 16(1)(pp 1-13), 2005. Date of Publication: Feb 2005.
Abstract
Selegiline is an irreversible inhibitor of monoamine oxidase (MAO) with psychostimulant and
neuroprotective effects. Several lines of evidence suggest that treatment with selegiline at
doses that exceed levels required for inhibition of MAO can produce distinct pharmacologic
effects. The purpose of this study was to evaluate the effects of chronic treatment with highdose selegiline on extinction responding, cue-induced reinstatement, morphine reinforcement
and naloxone-precipitated withdrawal. After pretreatment with noncontingent morphine to
establish opiate dependence, rats acquired self-administration of 3.2 mg/kg per injection of
morphine under a progressive ratio schedule. Daily treatment with saline or 6.4 mg/kg per day
of selegiline was then administered over extinction, reinstatement and re-acquisition of
morphine self-administration. To enhance or diminish the potential for psychostimulant
effects, selegiline was administered either immediately prior to (pre-session) or 1 h following
(post-session) extinction, reinstatement and; self-administration sessions. Pre-session
selegiline decreased the number of ratios completed on days 2, 3 and 4 of extinction, and
decreased morphine self-administration during all four re-acquisition sessions. When
administered at the same dose level, post-session selegiline decreased responding on the
fourth extinction session, and was ineffective in modifying re-acquisition of self-administration.
Selegiline administered by either schedule did not modify cue-induced reinstatement. Daily
treatment with 6.4 mg/kg per day of selegiline did not modify self-administration of food under
a progressive ratio schedule. Acute treatment with single, 6.4 mg/kg doses of selegiline
attenuated naloxone-induced increases in ptosis and global withdrawal score, but did not
modify any other sign of withdrawal or global withdrawal score calculated without ratings of
ptosis. In conclusion, high-dose selegiline can attenuate extinction responding and morphinereinforced behavior, and these effects may be mediated by psychostimulant metabolites.
copyright 2005 Lippincott Williams & Wilkins.
ISSN 0955-8810
Publication Type Journal: Article
Journal Name Behavioural Pharmacology
Volume 16
Issue Part 1
Page 1-13
Year of Publication 2005
Date of Publication Feb 2005
OPIOIDS <467>
Database EMBASE
Accession Number 2005115753
Authors Porzionato A. Macchi V. Guidolin D. Parenti A. Ferrara S.D. De Caro R.
Institution
(Macchi, Guidolin, De Caro) Dept. of Hum. Anatomy and Physiology, Section of Anatomy, University of Padova,
Padova, Italy.
(Parenti) Dept. of Oncological and Surg. Sci., Section of Pathologic Anatomy, University of Padova, Padova, Italy.
(Porzionato, Ferrara) Environ. Medicine and Public Health, Section of Legal Medicine, University of Padova,
Padova, Italy.
(De Caro) Dept. of Hum. Anatomy and Physiology, Section of Anatomy, Via A. Gabelli 65, 35121 Padova, Italy.
Country of Publication
United Kingdom
Title
Histopathology of carotid body in heroin addiction. Possible chemosensitive
impairment.
Source
Histopathology. 46(3)(pp 296-306), 2005. Date of Publication: Mar 2005.
Abstract
Aims: To perform a morphometric analysis of carotid bodies in opiate addicts. Methods and
results: Carotid bodies were sampled at autopsy from 35 subjects who died of heroin
intoxication (mean age 26 years), and from eight young (22 years) and eight older subjects
(66.5 years) who died of trauma. Sections were stained with haematoxylineosin, azanMallory, and double-labelling immunohistochemistry with antineuronal specific enolase and
anti-S100, to count type I and type II cells. Interlobular and intralobular connective tissue was
increased both in the opiate cases (43.45 +/- 6.79%, P < 0.001. and 13.34 +/- 5.72%, P <
0.001, respectively) and older cases (46.67 +/- 1.65%, P < 0.001, and 9.62 +/- 2.11%, P <
0.05, respectively) compared with young cases (33.17 +/- 6.41% and 4.33 +/- 1.84%,
respectively). The percentage of type II cells in the opiate cases (51.6 +/- 7.3%, P < 0.001)
and in the older controls (49.0 +/- 7.2%, P < 0.01) was higher than in the young cases (37.9
+/- 3.0%). Among type I cells, the light cell percentage in the opiate cases (65.85 +/- 11%, P <
0.001) was reduced with respect to the two control groups (82.8 +/- 5.34%, young: 81.62 +/8.58%, older). Conclusions: The increases in connective tissue and type II cells are similar to
findings in ageing and chronic pulmonary disease, and may be ascribed to glomic hypoxia. A
direct action of opiates should be taken into account for the decrease in light cells in heroin
addiction. The histopathological changes in the carotid body, by impairing chemosensivity,
may play a role in the fatal cardiorespiratory derangement of heroin addicts. copyright 2005
Blackwell Publishing Limited.
ISSN 0309-0167
Publication Type Journal: Article
Journal Name Histopathology
Volume 46
Issue Part 3
Page 296-306
Year of Publication 2005
Date of Publication Mar 2005
OPIOIDS <468>
Database EMBASE
Accession Number 2005114955
Authors Sorensen H.J. Jepsen P.W. Haastrup S. Juel K.
Institution
(Sorensen) Danish Epidemiology Science Centre, Institute of Preventive Medicine, Copenhagen Hospital
Corporation, Copenhagen, Denmark.
(Sorensen) Department of Psychiatry, Copenhagen University Hospital, Amager, Denmark.
(Jepsen) Department of Psychiatry, Copenhagen University Hospital, Rigshospitalet,
(Haastrup) Department of Psychiatry, Copenhagen University Hospital, Glostrup, Denmark.
(Juel) National Institute of Public Health, Copenhagen, Denmark.
(Jepsen) Dist. Mental Health Centre Indre By, Vestergade 27, DK-1456 Copenhagen K, Denmark.
Country of Publication
United Kingdom
Title
Drug-use pattern, comorbid psychosis and mortality in people with a history of opioid
addiction.
Source
Acta Psychiatrica Scandinavica. 111(3)(pp 244-249), 2005. Date of Publication: Mar 2005.
Abstract
Objective: To compare the 15-year mortality of people with a history of opioid dependence
that had achieved stable abstinence, with the mortality associated with continued drug use.
Another objective was to study the influence of hospitalization with comorbid psychosis on the
15-year mortality. Method: In 1984, 188 persons (122 men and 66 women) with a history of
intravenous narcotics addiction were interviewed about their drug-use pattern. A registrybased follow-up continued through 1999 and mortality was assessed. Three 1984-drug-use
categories were formed. In category 1, cohort members had achieved stable abstinence from
drug use by 1984. Using Cox multiple regression analysis, we (i) estimated reduced mortality
of category 1 drug users, and (ii) studied the influence of hospitalization with comorbid
psychosis on mortality. Results: About 32% had died during the 15-year follow-up. The 15year mortality associated with stable abstinence was reduced by 56% when compared with
the perceived worst drug-use pattern. Hospitalization for comorbid psychosis was not
independently associated with mortality in this sample. When drug-use categories were
compared with mortality expectations for the general population, the standard mortality rates
(SMRs) were clearly elevated. Even in the stably abstinent drug-use category (category 1),
SMR was significantly elevated by at least seven-fold in both genders. Conclusion: People
who had achieved stable abstinence from injecting narcotics use were at lower risk of
premature death than people with continued drug use. A residual observed excess mortality
in people who had apparently achieved stable abstinence from drug use is consistent with the
view of drug addiction as a chronic disease. copyright Blackwell Munksgaard 2004.
ISSN 0001-690X
Publication Type Journal: Article
Journal Name Acta Psychiatrica Scandinavica
Volume 111
Issue Part 3
Page 244-249
Year of Publication 2005
Date of Publication Mar 2005
OPIOIDS <472>
Database EMBASE
Accession Number 2005103102
Authors Jage J.
Institution
(Jage) Department of Anaesthesiology, University Hospital, Johannes Gutenberg-University Mainz, Langenbeckstr.
1, 55131 Mainz, Germany.
Country of Publication
United Kingdom
Title
Opioid tolerance and dependence - Do they matter?
Source
European Journal of Pain. 9(2 SPEC. ISS.)(pp 157-162), 2005. Date of Publication: Apr
2005.
Abstract
The use of opioids has long been accepted as the standard of care in patients with cancer
and acute pain. Opioids can further be used effectively in specific subgroups of patients with
chronic nonmalignant pain states. While the development of tolerance and physical
dependence are known effects of opioids in cancer and noncancer pain populations, these
patients can not be regarded as addicted. However, long-term therapy with short-acting
opioids predisposes to tolerance and addiction. Recent research has confirmed the important
role of psychopathologic and psychosocial conditions as predictors of failed opioid
effectiveness in a significant number of noncancer pain subgroups. The clinical picture of
failed therapy may be complicated by noncompliance, concealed consumption of
psychotropic substances, and diversion of prescribed opioids for various purposes as, e.g.,
selling for profit, or sharing excess opioids with others. This article discusses the effects of
opioid therapy, including tolerance, physical dependence, drug-aberrant behavior, drug
history, psychopathology, and somatization. copyright 2004 European Federation of Chapters
of the International Association for the Study of Pain. Published by Elsevier Ltd. All rights
reserved.
ISSN 1090-3801
Publication Type Journal: Article
Journal Name European Journal of Pain
Volume 9
Issue Part 2 SPEC. ISS.
Page 157-162
Year of Publication 2005
Date of Publication Apr 2005
OPIOIDS <474>
Database EMBASE
Accession Number 2005093533
Authors Aldhous P.
Country of Publication
United Kingdom
Title
Cold turkey, Vietnamese style.
Source
Nature. 433(7026)(pp 568-569), 2005. Date of Publication: 10 Feb 2005.
Abstract
It was invented by a healer familiar with the horrors of opiate addiction, and refined by
Vietnam's leading chemistry lab. Can this novel herbal cocktail ease withdrawal and reduce
drug cravings? Peter Aldhous investigates.
ISSN 0028-0836
Publication Type Journal: Short Survey
Journal Name Nature
Volume 433
Issue Part 7026
Page 568-569
Year of Publication 2005
Date of Publication 10 Feb 2005
OPIOIDS <477>
Database EMBASE
Accession Number 2005088328
Authors Shewan D. Dalgarno P.
Institution
(Shewan, Dalgarno) Glasgow Caledonian University, Glasgow, United Kingdom.
(Shewan) Department of Psychology, Glasgow Caledonian University, City Campus, Cowcaddens Road, Glasgow
G4 0BA, United Kingdom.
Country of Publication
United Kingdom
Title
Evidence for controlled heroin use? Low levels of negative health and social
outcomes among non-treatment heroin users in Glasgow (Scotland).
Source
British Journal of Health Psychology. 10(1)(pp 33-48), 2005. Date of Publication: Feb 2005.
Abstract
Objectives. This longitudinal study focused on 126 long-term heroin users who had never
been in specialist treatment for use of any drug. The primary aim of the study was to assess
whether this 'hidden' population resembled heroin users identified with drug treatment
agencies, or alternatively, to test whether heroin could indeed be used in a controlled, nonintrusive fashion for an extended period of time. Design and methods. Recruitment was
achieved through chain-referred purposive sampling methods, and data were collected
through two semi-structured interviews. 67% of participants were re-recruited for follow-up.
Results. Participants had levels of occupational status and educational achievement
comparable to that in the general UK population, and considerably higher than typically found
in heroin research. At the conclusion of the study, six participants had entered treatment.
While there was evidence of intensive risky patterns of drug use among the sample, there
was equal evidence for planned, controlled patterns of use. Some drug-related negative
health and social outcomes had occurred on a lifetime basis, but ongoing problems were rare,
and heroin was not a significant predictor in either context. In contrast to typical samples of
heroin users, high levels of negative health and social outcomes did not appear to be
inevitable within this sample. Frequency of heroin use was predicted by attributional items,
indicating the importance of psychological factors in drug use and addiction. Conclusions.
Drug research should more fully incorporate previously hidden populations to more fully
inform theory and practice. The pharmacological properties of specific substances should not
be assumed to inevitably lead to addictive and destructive patterns of drug use.
ISSN 1359-107X
Publication Type Journal: Article
Journal Name British Journal of Health Psychology
Volume 10
Issue Part 1
Page 33-48
Year of Publication 2005
Date of Publication Feb 2005
OPIOIDS <478>
Database EMBASE
Accession Number 2005083929
Authors De Jong C.A.J. Laheij R.J.F. Krabbe P.F.M.
Institution
(De Jong) Novadic - Kentron - Netwk. A., Nijmegen Inst. S., Radboud University Nijmegen, Nijmegen, Netherlands.
(Laheij, Krabbe) Dept. of Med. Technology Assessment, University Medical Centre Nijmegen, Nijmegen,
Netherlands.
(De Jong) Novadic - Kentron - Netwk. A., Nijmegen Inst. S., Radboud University Nijmegen, PO Box 9104, 6500 HE
Nijmegen, Netherlands.
Country of Publication
United Kingdom
Title
General anaesthesia does not improve outcome in opioid antagonist detoxification
treatment: A randomized controlled trial.
Source
Addiction. 100(2)(pp 206-215), 2005. Date of Publication: Feb 2005.
Abstract
Aim: Opioid detoxification by administering opioid-antagonists under general anaesthesia
has caused considerable controversy. This study is conducted to determine whether rapid
detoxification under general anaesthesia results in higher levels of opioid abstinence than
rapid detoxification without anaesthesia. Design: Randomized controlled open clinical trial
from September 1999 to August 2001. Setting: Four addiction centres in collaboration with
three general hospitals in the Netherlands. Participants: A total of 272 opioid-dependent
patients whose previous attempts to abstain were unsuccessful. Intervention: Patients
received rapid detoxification with general anaesthesia (RD-GA) or without general
anaesthesia (RD). Measurements: Urine screens and an interview (EuropASI) to assess
opioid abstinence two questionnaires (SOOS, OOWS) to measure withdrawal symptoms and
one to measure craving (VAS). Findings: One month after the intervention 62.8% of the
patients in the RD-GA group and 60.0% in the RD group were abstinent for opioids (P =
0.71). No adverse events or complications occurred during RD; however, in the RD-GA
group, five adverse events necessitated admission to a general hospital. The average 1month cost for RD was [euro]2517 versus [euro]4439 for RD-GA. Conclusions: Rapid
detoxification under general anaesthesia did not result in higher levels of opioid abstinence
than rapid detoxification without anaesthesia. The cost of the former intervention was much
higher.
ISSN 0965-2140
Publication Type Journal: Article
Journal Name Addiction
Volume 100
Issue Part 2
Page 206-215
Year of Publication 2005
Date of Publication Feb 2005
OPIOIDS <481>
Database EMBASE
Accession Number 2005079225
Authors Simoens S. Matheson C. Bond C. Inkster K. Ludbrook A.
Institution
(Simoens) Drug and Patient Information, Faculty of Pharmaceutical Sciences, Katholieke Universiteit Leuven,
Edward van Evenstraat 4, 3000 Leuven, Belgium.
(Matheson, Bond, Inkster) Dept. of Gen. Practice/Primary Care, University of Aberdeen, Aberdeen, United Kingdom.
(Ludbrook) Health Economics Research Unit, University of Aberdeen, Aberdeen, United Kingdom.
Country of Publication
United Kingdom
Title
The effectiveness of community maintenance with methadone or buprenorphine for
treating opiate dependence.
Source
British Journal of General Practice. 55(511)(pp 139-146), 2005. Date of Publication: Feb
2005.
Abstract
Background. Opiate dependence is a major health and social issue in many countries. A
mainstay of therapy has been methadone maintenance treatment, but other treatments,
particularly buprenorphine, are increasingly being considered. Aim. To conduct a systematic
review to synthesise and critically appraise the evidence on the effectiveness of community
maintenance programmes with methadone or buprenorphine in treating opiate dependence.
Method. A systematic review of databases, journals and the grey literature was carried out
from 1990-2002. Inclusion criteria were: community-based, randomised controlled trials of
methadone and/or buprenorphine for opiate dependence involving subjects who were aged
18 years old or over. Results. Trials were set in a range of countries, employed a variety of
comparators, and suffered from a number of biases. The evidence indicated that higher doses
of methadone and buprenorphine are associated with better treatment outcomes. Low-dose
methadone (20 mg per day) is less effective than buprenorphine (2-8 mg per day). Higher
doses of methadone (>50-65 mg per day) are slightly more effective than buprenorphirie (2-8
mg per day). There was some evidence that primary care could be an effective setting to
provide this treatment, but such evidence was sparse. Conclusion. The literature supports the
effectiveness of substitute prescribing with methadone or buprenorphine in treating opiate
dependence. Evidence is also emerging that the provision of methadone or buprenorphine by
primary care physicians is feasible and may be effective. copyright British Journal of General
Practice 2005.
ISSN 0960-1643
Publication Type Journal: Review
Journal Name British Journal of General Practice
Volume 55
Issue Part 511
Page 139-146
Year of Publication 2005
Date of Publication Feb 2005
OPIOIDS (A) <484>
Database EMBASE
Accession Number 2005069433
Authors Rasmussen K. Martin H. Berger J.E. Seager M.A.
Institution
(Rasmussen, Seager) Lilly Research Laboratories, Eli Lilly and Co., Lilly Corporate Center, Indianapolis, IN 46285,
United States.
(Martin, Berger) Coll. of Pharm. and Health Sciences, Butler University, Indianapolis, IN 46028, United States.
Country of Publication
United Kingdom
Title
The mGlu5 receptor antagonists MPEP and MTEP attenuate behavioral signs of
morphine withdrawal and morphine-withdrawal-induced activation of locus coeruleus
neurons in rats.
Source
Neuropharmacology. 48(2)(pp 173-180), 2005. Date of Publication: Feb 2005.
Abstract
N-Methyl-D-aspartate (NMDA) antagonists have been demonstrated to suppress the signs
of opiate withdrawal; however, side effects limit their clinical use. Since the metabotropic
glutamate (mGlu) 5 receptor has been shown to affect glutamate release and modulate
NMDA receptor function, we examined the effects of two selective mGlu5 receptor
antagonists, 2-methyl-6-(phenyl-ethynyl)- pyridine (MPEP) and 3-[(2-methyl-1,3-thiazol-4yl)ethynyl]pyridine (MTEP), on morphine withdrawal. Pretreatment with MPEP or MTEP (1, 3,
and 10 mg/kg, i.p.) significantly attenuated behavioral signs of morphine withdrawal.
Specifically, both MPEP and MTEP attenuated the occurrence/severity of chews, digging,
salivation, and weight loss, and increased the occurrence of erections. Neither compound
changed the occurrence of wet-dog shakes, ptosis, irritability, or lacrimation. Both MPEP and
MTEP produced a modest, but significant, attenuation of morphine-withdrawal-induced
activation of locus coeruleus neurons in anesthetized rats. These results indicate a role for
mGlu5 receptors in morphine withdrawal and suggest the potential for mGlu5 antagonists in
the treatment of withdrawal from opiates and other drugs of abuse. copyright 2004 Elsevier
Ltd. All rights reserved.
ISSN 0028-3908
Publication Type Journal: Article
Journal Name Neuropharmacology
Volume 48
Issue Part 2
Page 173-180
Year of Publication 2005
Date of Publication Feb 2005
OPIOIDS <489>
Database EMBASE
Accession Number 2005051472
Authors Larrinaga G. Gil J. Meana J.J. Ruiz F. Callado L.F. Irazusta J.
Institution
(Larrinaga) Department of Nursing I, University of the Basque Country, Leioa, P.O. Box 699, E-48940 Bilbao,
Bizkaia, Spain.
(Gil, Ruiz, Irazusta) Department of Physiology, University of the Basque Country, Spain.
(Meana, Callado) Department of Pharmacology, University of the Basque Country, Spain.
Country of Publication
United Kingdom
Title
Aminopeptidase activity in the postmortem brain of human heroin addicts.
Source
Neurochemistry International. 46(3)(pp 213-219), 2005. Date of Publication: Feb 2005.
Abstract
Several studies have reported that the chronic administration of opioids induces changes in
the biosynthesis of endogenous opioid peptides or their precursors in specific brain regions of
the adult central nervous system. However, little is known about the catabolic regulation of
opioid peptides and its contribution to neuroadaptative changes underlying drug addiction. In
the present study, we have analyzed the activity of two enkephalin-degrading enzymes
(puromycin-sensitive aminopeptidase or PSA and aminopeptidase N or APN) and two
functionally different, soluble aminopeptidases (aminopeptidase B and aspartylaminopeptidase) in postmortem samples of prefrontal cortex and caudate nucleus of eight
human heroin addict brains and eight matched-controls. Enzyme activities were
fluorimetrically measured using beta-naphthylamide derivatives. An increase in the activity of
soluble PSA in the prefrontal cortex of heroin abusers was observed (heroin addict group:
51,452 +/- 3892 UAP/mg protein versus control group: 42,003 +/- 2597 UAP/mg protein; P <
0.05), while the activity of the other peptidases in both brain regions remained unaltered. This
result agrees with previous findings in morphine-tolerant rats, and indicates that soluble PSA
may be involved in neurobiological processes which underlie heroin addiction. copyright 2004
Elsevier Ltd. All rights reserved.
ISSN 0197-0186
Publication Type Journal: Article
Journal Name Neurochemistry International
Volume 46
Issue Part 3
Page 213-219
Year of Publication 2005
Date of Publication Feb 2005
OPIOIDS <491>
Database EMBASE
Accession Number 2005050645
Authors Damen K.F.M. Dejong C.A.J. Breteler M.H.M. Vanderstaak C.P.F.
Institution
(Damen, Dejong, Breteler, Vanderstaak) Nijmegen Inst. Sci. Practitioners, Montessorilaan 10, 6525 HR Nijmegen,
Netherlands.
Country of Publication
United Kingdom
Title
Construct validity of the SIDP-IV in an opioid-dependent patient sample.
Source
Journal of Substance Use. 10(1)(pp 1-9), 2005. Date of Publication: Feb 2005.
Abstract
Aims: Studies on opioid-dependent patients, report high comorbidity with personality
pathology. Since psychiatric comorbidity is related to poorer treatment outcome and drop-out
in opioid-dependent patients, in this study, the underlying structure of the DSM-IV personality
disorders in an opioid-dependent patient sample (n=263), assessed by the structured
interview for DSM-IV Personality, was explored in order to contribute to the construct validity
of this instrument. Design: Explorative factor analysis yielded a three-factor solution, largely
resembling the DSM-IV cluster model. Findings: The optional disorders, depressive and
negativistic personality disorder, did not detract from the presumed model. Confirmatory
factor analysis did not confirm a good fit of the model to the data, which is due to the paranoid
personality disorder (PD) which groups with cluster B PDs. Conclusions: Overall, the
underlying structure of DSM-IV PDs resembles the presumed DSM-IV cluster model, thereby
suggesting good construct validity of the SIDP-IV in opioid-dependent patients. copyright
2005 Taylor & Francis Group Ltd.
ISSN 1465-9891
Publication Type Journal: Article
Journal Name Journal of Substance Use
Volume 10
Issue Part 1
Page 1-9
Year of Publication 2005
Date of Publication Feb 2005
OPIOIDS <495>
Database EMBASE
Accession Number 2005048575
Authors Ammon-Treiber S. Hollt V.
Institution
(Ammon-Treiber, Hollt) Inst. of Pharmacology and Toxicology, Otto-von-Guericke University, Magdeburg, Germany.
(Ammon-Treiber) Inst. of Pharmacology and Toxicology, Otto-von-Guericke Univ. Magdeburg, Leipziger Str. 44, D39120 Magdeburg, Germany.
Country of Publication
United Kingdom
Title
Morphine-induced changes of gene expression in the brain.
Source
Addiction Biology. 10(1)(pp 81-89), 2005. Date of Publication: Mar 2005.
Abstract
Repeated opiate administration alters gene expression in different brain regions of rodents,
an effect which may contribute to plastic changes associated with addictive behaviour. There
is increasing evidence that multiple transcription factors are induced in morphine tolerance,
sensitization and during morphine withdrawal. Whereas morphine treatment does not lead to
major alterations in the expression of mu-opioid receptors (MOR), there is transcriptional
regulation of proteins involved in MOR trafficking such as GRK2 or beta arrestin 2 as well as
altered expression of other receptors such as dopamine receptors, NMDA receptors,
GABA_A receptor and alpha _2A adrenoceptor. Recent gene
expression profiling studies reveal additional clusters of morphine-responsive genes: whereas
single dose administration has been shown to predominantly reduce expression of genes
involved in metabolic function, ascending morphine doses leading to morphine tolerance
revealed induction of genes which alter patterns of synoptic connectivity such as arc or ania3. These genes remained elevated after precipitated withdrawal, which also triggered the
expression of several transcriptional activators and repressors. In addition, morphine has
been shown to be a strong inducer of heat shock protein 70, a cell protective protein which
might counter-regulate opiate-induced neurotoxicity. Temporal expression profiles during a
chronic morphine application schedule revealed discrete and fluctuating expression of gene
clusters such as transcription factors, G-protein-coupled receptors and neuropeptides.
Prolonged abstinence seems to be characterized by up-regulation of several transcription
factors and persistent down-regulation of ligand gated ion channels such as glutamatergic
and GABA-ergic receptor subunits. These long-term changes in receptor expression suggest
a persistent alteration of synaptic signalling after morphine treatment.
ISSN 1355-6215
Publication Type Journal: Article
Journal Name Addiction Biology
Volume 10
Issue Part 1
Page 81-89
Year of Publication 2005
Date of Publication Mar 2005
OPIOIDS (A) <497>
Database EMBASE
Accession Number 2005039578
Authors Wang Y. Wan C. Zhou W. Peng T. Liu Y. Wang Z. Li G. Cornelisson G. Halberg F.
Institution
(Liu, Wang, Wan, Zhou, Peng, Liu, Wang) West China Medical Center, Sichuan University, Chengdu, Sichuan
610041, China.
(Li) Nanchong Central Hospital, Nanchong, Sichuan 637000, China.
(Cornelisson, Halberg) Halberg Chronobiology Center, University of Minnesota, Minneapolis, MN 55455, United
States.
Country of Publication
United Kingdom
Title
The role of mPer1 in morphine dependence in mice.
Source
Neuroscience. 130(2)(pp 383-388), 2005. Date of Publication: 2005.
Abstract
Investigations using Drosophila melanogaster have shown that the circadian clock gene
period can influence behavioral responses to cocaine, and the mouse homologues, mPer1
and mPer2, modulate cocaine sensitization and reward. In the present study, we applied
DNAzyme targeting mPer1 to interfere the expression of mPer1 in CNS in mice and studied
the role of mPer1 on morphine dependence. We found that the DNAzyme could attenuate the
expression of mPer1 in CNS in mice. Mice treated with DNAzyme and morphine
synchronously did not show preference to the morphine-trained side, whereas the control
group did. In contrast, mice treated with DNAzyme after morphine showed preference to the
morphine-trained side as well as the control group did. These results indicate that drug
dependence seems to be influenced at least partially by mPer1, but mPer1 cannot affect
morphine dependence that has been formed. copyright 2004 IBRO. Published by Elsevier
Ltd. All rights reserved.
ISSN 0306-4522
Publication Type Journal: Article
Journal Name Neuroscience
Volume 130
Issue Part 2
Page 383-388
Year of Publication 2005
Date of Publication 2005
OPIOIDS <500>
Database EMBASE
Accession Number 2005038698
Authors Bailey C.P. Connor M.
Institution
(Bailey) Department of Pharmacology, University of Bristol, School of Medical Sciences, Bristol BS8 1TD, United
Kingdom.
(Connor) Pain Management Research Institute, University of Sydney, Royal North Shore Hospital, St. Leonards,
NSW 2065, Australia.
Country of Publication
United Kingdom
Title
Opioids: Cellular mechanisms of tolerance and physical dependence.
Source
Current Opinion in Pharmacology. 5(1)(pp 60-68), 2005. Date of Publication: Feb 2005.
Abstract
Morphine and other opioids are used and abused for their analgesic and rewarding
properties. Tolerance to these effects develops over hours/days to weeks, as can physical
and psychological dependence. Despite much investigation, the precise cellular mechanisms
underlying opioid tolerance and dependence remain elusive. Recent studies examining muopioid receptor desensitization and trafficking have revealed several potential mechanisms for
acute receptor regulation. Other studies have reported changes in many other proteins that
develop during chronic opioid treatment or withdrawal and such changes may be partly
responsible for the cellular and synaptic adaptations to prolonged opioid exposure. W hile
these studies have added to our knowledge of the cellular processes participating in opioid
tolerance and dependence, the challenge remains to integrate these observations into a
coherent explanation of the complex changes observed in whole animals chronically exposed
to opioids. copyright 2005 Elsevier Ltd. All rights reserved.
ISSN 1471-4892
Publication Type Journal: Review
Journal Name Current Opinion in Pharmacology
Volume 5
Issue Part 1
Page 60-68
Year of Publication 2005
Date of Publication Feb 2005
OPIOIDS <512>
Database EMBASE
Accession Number 2005006546
Authors Greenwald M.K. Roehrs T.A.
Institution
(Greenwald) Substance Abuse Research Division, Dept. of Psychiat./Behav. Neurosci., Wayne State Univ. School
of Medicine, Detroit, MI, United States.
(Roehrs) Sleep Disorders and Research Center, Henry Ford Hospital, Detroit, MI, United States.
(Greenwald) Substance Abuse Research Division, Dept. of Psychiat./Behav. Neurosci., Wayne State University,
2761 E Jefferson Ave, Detroit, MI 48207, United States.
Country of Publication
United Kingdom
Title
Mu-opioid self-administration vs passive administration in heroin abusers produces
differential EEG activation.
Source
Neuropsychopharmacology. 30(1)(pp 212-221), 2005. Date of Publication: Jan 2005.
Abstract
Psychoactive drug self-administration (SA) produces different neurobiological effects than
passive administration (PA) in non-human animals; however, such consequences have never
been
examined in
human drug abusers. The present study compared
electroencephalographic (EEG) activation produced by intravenous PA and SA of the muopioid fentanyl in eight heroin-dependent, methadone-stabilized male participants. In phase 1,
participants received cumulative PA of fentanyl (up to 1.5mg/70kg; session 1), then bolus PA
of placebo and fentanyl 1.5mg/70kg (session 2), High-dose fentanyl significantly increased
the amplitude of slow-frequency (delta- and theta-band) EEG activity. In phase 2, bolus
fentanyl 1.5 mg/70kg was available for SA, requiring the participant to complete 1500
responses, in each of two sessions after saline or naloxone pretreatment Delta EEG peak
amplitude increases were greater following fentanyl SA than fentanyl PA, primarily over the
central midline region, and were attenuated by naloxone pretreatment. The EEG increase and
its attenuation by naloxone agree with preclinical evidence and suggest that SA-related EEG
responses were mediated by opioid receptors.
ISSN 0893-133X
Publication Type Journal: Article
Journal Name Neuropsychopharmacology
Volume 30
Issue Part 1
Page 212-221
Year of Publication 2005
Date of Publication Jan 2005
OPIOIDS (A) <513>
Database EMBASE
Accession Number 2005006535
Authors Narita M. Kishimoto Y. Ise Y. Yajima Y. Misawa K. Suzuki T.
Institution
(Narita, Kishimoto, Ise, Yajima, Misawa, Suzuki) Department of Toxicology, Hoshi Univ. Sch. Pharm./P. S., Ebara,
Shinagawa-ku, Tokyo, Japan.
(Ise) Department of Pharmaceutical Service, Nippon Medical School Hospital, Sendagi Bunkyo-ku, Tokyo, Japan.
(Misawa) Narcotic Drugs/Psychotropic S. E. D., World Health Organization, Geneva, Switzerland.
(Narita, Suzuki) Department of Toxicology, Hoshi Univ. Sch. of Pharm./P. S., 2-4-41 Ebara, Shinagawa-ku, Tokyo
142-8501, Japan.
Country of Publication
United Kingdom
Title
Direct evidence for the involvement of the mesolimbic kappa-opioid system in the
morphine-induced rewarding effect under an inflammatory pain-like state.
Source
Neuropsychopharmacology. 30(1)(pp 111-118), 2005. Date of Publication: Jan 2005.
Abstract
Recent clinical studies have demonstrated that when morphine is used to control pain in
cancer patients, psychological dependence is not a major concern. The present study was
undertaken to ascertain the modulation of psychological dependence on morphine under a
chronic pain-like state in rats. The prototypical mu-opioid receptor agonist morphine (8 mg/kg,
i.p.) induced a dose-dependent place preference. In the present study, we found that an
inflammatory pain-like state following formalin injection significantly suppressed the morphineinduced rewarding effect. This effect was almost reversed by s.c. pretreatment with the
kappa-opioid receptor antagonist norbinaltorphimine (nor-BNI, 5 mg/kg). Furthermore, the
morphine-induced increase in dopamine (DA) turnover in the limbic forebrain was significantly
inhibited by treatment with formalin. This inhibition was also suppressed by pretreatment with
nor-BNI. In addition, in vivo microdialysis studies clearly showed that the morphine-induced
increase in the extracellular levels of DA and its metabolites, 3,4-dihydroxyphenylacetic acid
and homovanillic acid, in the nucleus accumbens (N.Acc.) was significantly decreased in rats
that had been pretreated with formalin. This effect was in turn reversed by the microinjection
of a specific dynorphin A antibody into the N.Acc. These findings suggest that the
inflammatory pain-like state induced by formalin injection may have caused a sustained
activation of the kappa-opioidergic system within the N.Acc., resulting in suppression of the
morphine-induced rewarding effect in rats. The present study provides further evidence of the
clinical usefulness of morphine in patients suffering from severe pain.
ISSN 0893-133X
Publication Type Journal: Article
Journal Name Neuropsychopharmacology
Volume 30
Issue Part 1
Page 111-118
Year of Publication 2005
Date of Publication Jan 2005
OPIOIDS (A) <514>
Database EMBASE
Accession Number 2005006534
Authors Lopez-Fando A. Rodriguez-Munoz M. Sanchez-Blazquez P. Garzon J.
Institution
(Lopez-Fando, Rodriguez-Munoz, Sanchez-Blazquez, Garzon) Neurofarmacologia, Inst. Neurbio. Santiago Ramon
Cajal, CSIC, Madrid, Spain.
(Garzon) Neurofarmacologia, Instituto Cajal, Consejo Sup. de Invest. Cientificas, Avd Doctor Arce, 37, Madrid E28002, Spain.
Country of Publication
United Kingdom
Title
Expression of neural RGS-R7 and Gbeta5 proteins in response to acute and chronic
morphine.
Source
Neuropsychopharmacology. 30(1)(pp 99-110), 2005. Date of Publication: Jan 2005.
Abstract
The R7 subfamily of regulators of G-protein signaling (RGS) proteins (RGS6, RGS7, RGS92, and RGS11), and its binding protein Gbeta5, are found in neural structures of mouse brain.
A single intracerebroventricular priming dose of 10 nmol morphine gave rise to acute
tolerance to the analgesic effects of successive identical test doses of the opioid. At 2 h after
administering the acute opioid, RGS7 mRNA levels in the striatum plus those of RGS9-2 in
the striatum and thalamus were increased, whereas RGS9-2 and RGS11 mRNA were
reduced in the cortex. Similar but attenuated RGS-R7 mRNA changes persisted 24h after
acute morphine administration. No changes in Gbeta5 mRNA levels were observed. At 2 days
after commencing sustained morphine treatment, the levels of mRNA for RGS7, RGS9-2,
RGS11, and Gbeta5 increased in most of the brain structures studied (striatum, thalamus,
periaqueductal gray matter (PAG), and cortex). In these morphine tolerant-dependent mice,
the greater changes were found for RGS9-2 in the thalamus (> 500%) and PAG (> 200%). In
post-dependent mice, the increases in RGS-R7 and Gbeta5 mRNA still persisted in the PAG
and striatum at 8 and 16 days after starting the chronic opioid treatment. The raised mRNA
levels promoted by chronic, but not by acute, morphine, were accompanied by increases in
the encoded proteins. This is probably a result of the costabilization of the RGS-R7 and
Gbeta5 proteins forming heterodimers. Opioid-induced adaptations of RGS-R7 and Gbeta5
genes may regulate the severity of morphine-induced tolerance/dependence and the duration
of the post-dependent period, helping to recover the normal response.
ISSN 0893-133X
Publication Type Journal: Article
Journal Name Neuropsychopharmacology
Volume 30
Issue Part 1
Page 99-110
Year of Publication 2005
Date of Publication Jan 2005
OPIOIDS (A) <515>
Database EMBASE
Accession Number 2005006533
Authors Stinus L. Cador M. Zorrilla E.P. Koob G.F.
Institution
(Stinus, Cador) Lab. Neuropsychobiol. Desadaptations, Universite de Bordeaux II, Bordeaux, Cedex, France.
(Zorrilla, Koob) Department of Neuropharmacology, Scripps Research Institute, San Diego, CA, United States.
(Stinus) Lab. Neuropsychobiol. Desadaptations, Universite de Bordeaux II, UMR-CNRS 5541, Bordeaux, Cedex
33076, France.
Country of Publication
United Kingdom
Title
Buprenorphine and a CRF₁ antagonist block the acquisition of opiate
withdrawal-induced conditioned place aversion in rats.
Source
Neuropsychopharmacology. 30(1)(pp 90-98), 2005. Date of Publication: Jan 2005.
Abstract
Conditioned place aversion in rats has face validity as a measure of the aversive stimulus
effects of opiate withdrawal that reflects an important motivational component of opiate
dependence. The purpose of the present study was to validate conditioned place aversion as
sensitive to medications that will alleviate the aversive stimulus effects of opiate withdrawal in
humans, and to extend this model to the exploration of the neuropharmacological basis of the
motivational effects of opiate withdrawal. Male Sprague-Dawley rats were implanted with two
subcutaneous morphine pellets and 5 days later began place conditioning training following
subcutaneous administration of a low dose of naloxone. Animals were subjected to three
pairings of a low dose of naloxone (15 mug/kg, s.c.) to one arm of a three-chambered place
conditioning apparatus, Buprenorphine administered prior to each pairing dose-dependently
blocked the place aversion produced by precipitated opiate withdrawal, A corticotropinreleasing factor-1 (CRF₁) receptor antagonist (antalarmin) also reversed the
place aversion produced by precipitated opiate withdrawal. Antalarmin did not produce a
place preference or place aversion by itself in morphine-dependent rats. No effect was
observed with pretreatment of the dopamine partial agonist terguride or the selective
serotonin reuptake inhibitor fluoxetine. Also, chronic pretreatment with acamprosate (a
glutamate receptor modulator used to prevent relapse in alcohol dependence) did not alter
naloxone-induced place aversion. Buprenorphine by itself in dependent rats produced a mild
place preference at low doses and a mild place aversion at higher doses. These results
suggest that buprenorphine blocks the aversive stimulus effects of precipitated opiate
withdrawal in rats and provides some validity for the use of place conditioning as a measure
that is sensitive to potential opiate-dependence medications. In addition, these results
suggest that CRF₁ antagonists can block the aversive stimulus effects of opiate
withdrawal and may be potential therapeutic targets for opiate dependence.
ISSN 0893-133X
Publication Type Journal: Article
Journal Name Neuropsychopharmacology
Volume 30
Issue Part 1
Page 90-98
Year of Publication 2005
Date of Publication Jan 2005
OPIOIDS <522>
Database EMBASE
Accession Number 2004504633
Authors Feroni I. Peretti-Watel P. Masut A. Coudert C. Paraponaris A. Obadia Y.
Institution
(Feroni, Peretti-Watel, Paraponaris, Obadia) Inst. Natl. de la Rech. Med., U 379, 23 Rue Stanislas Torrents, 13006,
Marseilles, France.
(Masut, Coudert) Caisse Natl. d'Assur. Malad. B., 56 Chemin Joseph Aiguier, Marseilles, France.
Country of Publication
United Kingdom
Title
French general practitioners' prescribing high-dosage buprenorphine maintenance
treatment: Is the existing training (good) enough?
Source
Addictive Behaviors. 30(1)(pp 187-191), 2005. Date of Publication: Jan 2005.
Abstract
In France, since 1996, any general practitioner (GP) can prescribe high-dosage
buprenorphine maintenance treatment (BMT) for opioid-dependent patients. The health
authorities initially provided mandatory specific training, but since 1998, such training is only
delivered by specialized networks and the pharmaceutical industry. Among a random sample
of GPs from southeastern France (N=345), we found that many untrained GPs, as well as a
significant minority of trained GPs, were likely to prescribe an ineffective dosage of
buprenorphine or a potentially dangerous treatment (BMT+a short half-life benzodiazepine).
These results highlight the necessity to edit clear guidelines, especially concerning situations
of polyaddiction and psychiatric comorbidity, and to extend and improve BMT training in
France with a renewed involvement of health authorities for quality control of such training.
They even suggest that GPs' participation to specialized training sessions should become a
mandatory prerequisite for prescribing BMT. copyright 2004 Elsevier Ltd. All rights reserved.
ISSN 0306-4603
Publication Type Journal: Article
Journal Name Addictive Behaviors
Volume 30
Issue Part 1
Page 187-191
Year of Publication 2005
Date of Publication Jan 2005
OPIOIDS (A) <525>
Database EMBASE
Accession Number 2004459697
Authors Grasing K. He S. Li N.
Institution
(Grasing, He, Li) Substance Abuse Research Laboratory, Kansas City Vet. Aff. Medical Center, 4801 Linwood
Blvd., Kansas City, M.,
(Grasing) Division of Clinical Pharmacology, Department of Medicine, Univ. Kansas Sch. Med., Kansas C.,
Country of Publication
United Kingdom
Title
Selegiline modifies the extinction of responding following morphine selfadministration, but does not alter cue-induced reinstatement, reacquisition of
morphine reinforcement, or precipitated withdrawal.
Source
Pharmacological Research. 51(1)(pp 69-78), 2005. Date of Publication: Jan 2005.
Abstract
Selegiline is an irreversible inhibitor of monoamine oxidase (MAO) with psychostimulant and
neuroprotective effects which can prevent decreases in dopamine efflux that follow opiate
withdrawal. The present study evaluated effects of selegiline treatment on morphine-seeking
behavior and morphine reinforcement in Wistar rats (n = 26). In additional animals (n = 30),
the ability of single doses of selegiline to modify naloxone-precipitated withdrawal was
determined. After pretreatment with noncontingent morphine to establish opiate dependence,
rats acquired self-administration of intravenous morphine. Daily intravenous treatment with
saline or 2.0 mg kg^-1 doses of selegiline was then initiated and continued over
14 days during extinction, reinstatement, and reacquisition of morphine self-administration. To
reduce the potential for psychostimulant effects, selegiline was administered approximately 1
h following self-administration, extinction, or reinstatement sessions. In some animals (n =
23), effects of saline or selegiline administration on locomotor activity were determined
following extinction sessions. Daily selegiline treatment decreased the number of ratios
completed and increased response latency during extinction, without modifying these
measures during reinstatement or reacquisition of morphine self-administration. Chronic
selegiline treatment increased locomotor activity recorded between 4 and 7 h after selegiline
administration on day 7 of extinction, but otherwise did not alter locomotor activity.
Pretreatment with single, 2.0 mg kg^-1 doses of selegiline did not modify
naloxone-precipitated withdrawal. In conclusion, pretreatment with selegiline produced only a
small decrease in responding during extinction of morphine self-administration and did not
modify cue-induced reinstatement of morphine-seeking behavior, reacquisition or morphine
reinforcement, or precipitated withdrawal. copyright 2004 Elsevier Ltd. All rights reserved.
ISSN 1043-6618
Publication Type Journal: Article
Journal Name Pharmacological Research
Volume 51
Issue Part 1
Page 69-78
Year of Publication 2005
Date of Publication Jan 2005
OPIOIDS <527>
Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)
Unique Identifier 20407977
Status In-Process
Authors Kreek MJ. Borg L. Ducat E. Ray B.
Authors Full Name
Kreek, Mary Jeanne. Borg, Lisa. Ducat, Elizabeth. Ray, Brenda.
Institution
Laboratory of the Biology of Addictive Diseases, The Rockefeller University, New York, NY 10065, USA.
kreek@rockefeller.edu
Title
Pharmacotherapy in the treatment of addiction: methadone.
Source
Journal of Addictive Diseases. 29(2):200-16, 2010 Apr.
Journal Name
Journal of Addictive Diseases
Other ID
Source: NLM. NIHMS179773 [Available on 04/01/11]
Source: NLM. PMC2885886 [Available on 04/01/11]
Country of Publication
England
Abstract
Methadone maintenance treatment (MMT) is the most widely available pharmacotherapy for
opioid addiction and has been shown to be an effective and safe treatment over a period of
40 years. Although women comprise approximately 40% of clients currently being treated in
MMT programs, comparatively little research geared specifically toward this group has been
published. This article begins with an overview of neurobiological studies on opioid addiction,
including a discussion of gender differences, followed by a review of the pharmacology of
methadone. The authors then examine the particular needs and differences of women being
treated in MMTs, including co-dependence with other substances, women's health issues,
and psychosocial needs unique to this population. Research shows that women have different
substance abuse treatment needs in comparison to their male counterparts. One New York
City MMT program that has attempted to address these differences is highlighted.
Publication Type Journal Article. Research Support, N.I.H., Extramural. Research Support, Non-U.S. Gov't.
Date of Publication 2010 Apr
Year of Publication 2010
Issue/Part 2
Volume 29
Page 200-16
OPIOIDS <528>
Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)
Unique Identifier 20535759
Status In-Process
Authors Brownstein JS. Green TC. Cassidy TA. Butler SF.
Authors Full Name Brownstein, John S. Green, Traci C. Cassidy, Theresa A. Butler, Stephen F.
Institution
Inflexxion Inc., Newton, MA 02464-1594, USA.
Title
Geographic information systems and pharmacoepidemiology: using spatial cluster
detection to monitor local patterns of prescription opioid abuse.
Source
Pharmacoepidemiology & Drug Safety. 19(6):627-37, 2010 Jun.
Journal Name
Pharmacoepidemiology & Drug Safety
Country of Publication
England
Abstract
PURPOSE: Understanding the spatial distribution of opioid abuse at the local level may
facilitate public health interventions. METHODS: Using patient-level data from addiction
treatment facilities in New Mexico from ASI-MV Connect, we applied geographic information
system (GIS) in combination with a spatial scan statistic to generate risk maps of prescription
opioid abuse and identify clusters of product- and compound-specific abuse. Prescribed
opioid volume data was used to determine whether identified clusters are beyond geographic
differences in availability. RESULTS: Data on 24 452 patients residing in New Mexico were
collected. Among those patients, 1779 (7.3%) reported abusing any prescription opioid (past
30 days). According to opioid type, 979 patients (4.0%) reported abuse of any hydrocodone,
1007 (4.1%) for any oxycodone, 108 (0.4%) for morphine, 507 (2.1%) for Vicodin or generic
equivalent, 390 (1.6%) for OxyContin, and 63 (0.2%) for MS Contin or generic equivalent.
Highest rates of abuse were found in the area surrounding Albuquerque with 8.6 patients
indicating abuse per 100 interviewed patients. We found clustering of abuse around
Albuquerque (P = 0.001; Relative Risk = 1.35, and a radius of 146 km). At the compound
level, we found that drug availability was partly responsible for clustering of prescription opioid
abuse. After accounting for drug availability, we identified a second foci of Vicodin abuse in
the southern rural portion of the state near Las Cruces, NM and El Paso, Texas and bordering
Mexico (RR = 2.1; P = 0.001). CONCLUSIONS: A better understanding of local risk
distribution may have implications for response strategies to future introductions of
prescription opioids.
Publication Type Journal Article. Research Support, N.I.H., Extramural. Research Support, Non-U.S. Gov't.
Date of Publication 2010 Jun
Year of Publication 2010
Issue/Part 6
Volume 19
Page 627-37
OPIOIDS 2005 <633>
Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)
Unique Identifier 16042795
Status PubMed-not-MEDLINE
Authors Gerevich J. Bacskai E. Farkas L. Danics Z.
Authors Full Name Gerevich, Jozsef. Bacskai, Erika. Farkas, Lajos. Danics, Zoltan.
Institution Addiction Research Institute, Budapest. gerevichj@axelero.hu
Title
A case report: Pavlovian conditioning as a risk factor of heroin 'overdose' death.
Source
Harm Reduction Journal. 2:11, 2005 Jul 25.
Journal Name
Harm Reduction Journal
Other ID
Source: NLM. PMC1196296
Country of Publication
England
Abstract
BACKGROUND: The authors present a case illustrating a mechanism leading directly to
death which is not rare but has received little attention. CASE PRESENTATION: The case
was evaluated by autopsy, investigation of morphine concentration in the blood, and clinical
data. The heroin dose causing the 'overdose' death of a young man who had previously been
treated a number of times for heroin addiction did not differ from his dose of the previous day
taken in the accustomed circumstances. The accustomed dose taken in a strange
environment caused fatal complications because the conditioned tolerance failed to operate.
The concentration of morphine in the blood did not exceed the level measured during earlier
treatment. CONCLUSION: These results are in line with the data in the literature indicating
that morphine concentrations measured in cases of drug-related death do not differ
substantially from those measured in cases where the outcome is not fatal. A knowledge of
the conditioning mechanism can contribute to prevention of fatal cases of a similar type. The
harm reduction approach places great stress on preventive intervention based on data related
to drug-related death.
Publication Type Journal Article.
Date of Publication 2005 Jul 25
Year of Publication 2005
Volume 2
Page 11
OPIOIDS 2005 <944>
Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)
Unique Identifier 16323564
Status MEDLINE
Authors Frenois F. Le Moine C. Cador M.
Authors Full Name Frenois, Francois. Le Moine, Catherine. Cador, Martine.
Institution
Interactions Neuronales et Comportements, Universite Victor Segalen, Bordeaux, France. ffrenois@bordeaux.inra.fr
Title
The motivational component of withdrawal in opiate addiction: role of associative
learning and aversive memory in opiate addiction from a behavioral, anatomical and
functional perspective. [Review] [154 refs]
Source
Reviews in the Neurosciences. 16(3):255-76, 2005.
Journal Name
Reviews in the Neurosciences
Country of Publication
England
Abstract
A major challenge in current drug addiction research is not only to understand the immediate
effects of drugs of abuse on brain operations, but also to define at the behavioral and neural
levels how cognitive, emotional and motivational processes interact with drug use in order to
lead to this psychopathological state which defines addiction. It is now clear that factors other
than the direct effects of drugs of abuse are able to powerfully affect drug-seeking and drugtaking behaviors. In former opiate addicts, re-exposure to environmental situations previously
paired with withdrawal is able to induce strong craving episodes. It has been proposed that
these conditioned stimuli could be strongly involved in precipitating relapse in drug-taking
behavior by re-activating the neurobiological circuits which are engaged in an unconditioned
way by the withdrawal state itself, leading to a powerful aversive state relieved by drug
consumption renewal. In the present review, we provide evidence from a
neuropsychopharmacological viewpoint that environmental situations previously paired with
the opiate withdrawal syndrome might be able to maintain drug-seeking motivation. Using
behavioral models which allow assessment of the aversive and motivational properties of
opiate withdrawal both in the unconditioned and conditioned situations, we have recently
investigated using extensive mapping the neurobiological correlates which underlie acute
withdrawal and the trace of its memory in the brain in terms of localization and neuronal
population involved, with an anatomical and functional approach. Thus, on the basis of our
results, and together with a number of data in the literature, we provide a functional model for
the formation and retrieval of opiate withdrawal memories. [References: 154]
ISSN Print 0334-1763
Publication Type Journal Article. Research Support, Non-U.S. Gov't. Review.
Date of Publication 2005
Year of Publication 2005
Issue/Part 3
Volume 16
Page 255-76
OPIOIDS 2005 <946>
Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)
Unique Identifier 16262036
Status MEDLINE
Authors Graham CH. Meechan JG.
Authors Full Name Graham, Caroline H. Meechan, John G.
Institution
School of Dental Sciences, University of Newcastle upon Tyne, Newcastle upon Tyne, UK.
Title
Dental management of patients taking methadone.
Source
Dental Update. 32(8):477-8, 481-2, 485, 2005 Oct.
Journal Name
Dental Update
Country of Publication
England
Abstract
Methadone is a synthetic opiate used in the treatment of opiate addiction. Various sideeffects have been associated with the use of methadone. These include xerostomia, which
can contribute to a high caries rate. The UK Regional Drug Misuse Database reported that
around 118,500 drug users were receiving treatment from drug misuse agencies and GPs.
The vast majority (87%) were receiving treatment from community specialist services. As
many drug abusers have poor oral health, general dental practitioners are likely to encounter
such individuals. It is essential therefore that dentists are aware of the potential difficulties that
may be encountered when treating subjects receiving methadone. These problems may
relate to previous drug abuse and to the effects of methadone therapy.
ISSN Print 0305-5000
Publication Type Journal Article.
Date of Publication 2005 Oct
Year of Publication 2005
Issue/Part 8
Volume 32
Page 477-8, 481-2, 485
OPIOIDS (A) 2005 <964>
Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)
Unique Identifier 16011579
Status MEDLINE
Authors Szumlinski KK. Lominac KD. Frys KA. Middaugh LD.
Authors Full Name Szumlinski, K K. Lominac, K D. Frys, K A. Middaugh, L D.
Institution
Department of Physiology and Neuroscience, and Department of Psychiatry and Behavioral Sciences, Center for
Drug and Alcohol Programs, Medical University of South Carolina, Charleston, SC, USA. szumlink@musc.edu
Title
Genetic variation in heroin-induced changes in behaviour: effects of B6 strain dose
on conditioned reward and locomotor sensitization in 129-B6 hybrid mice.
Source
Genes, Brain, & Behavior. 4(5):324-36, 2005 Jul.
Journal Name
Genes, Brain, & Behavior
Country of Publication
England
Abstract
Substantial interindividual variability exists in the propensity to develop opiate addiction.
Genetic variation in opiate reward may contribute to this variability. A large body of evidence
indicates genetic variation in mice for several effects of opiate drugs. The present study
examined heroin-induced place conditioning and locomotor sensitization in the two strains of
mice employed most frequently in the generation of transgenic animals, C57BL/6J (B6) and
129X1/sVJ (129), as well as in groups of B6-129 hybrid mice, differing in their amount of B6
genetic background. Four pairings of 100 microg/kg of heroin elicited robust place
conditioning and locomotor sensitization in B6 controls and in N(10) congenic B6-129 hybrid
mice. In comparison, the identical treatment produced no locomotor sensitization and induced
place aversion in 129 controls. No heroin-induced changes in the behaviour of N(3) congenic
B6-129 hybrid mice or F5-8 non-congenic B6-129 hybrid mice were observed. The expression
of place conditioning was not facilitated in any group by the administration of a heroin-priming
injection prior to testing. These data indicate that genetic variation exists in mice for the
rewarding and locomotor-sensitizing effects of heroin and that the capacity of heroin to induce
conditioned reward and locomotor sensitization can be modulated in a B6 strain dosedependent manner in B6-129 hybrid mice. Thus, strain differences in heroin responsiveness
should be considered when examining transgenic lines on B6-129 backgrounds for opiateinduced changes in behaviour that may be relevant for addiction.
ISSN Print 1601-1848
Publication Type Comparative Study. Journal Article. Research Support, N.I.H., Extramural. Research Support,
Non-U.S. Gov't. Research Support, U.S. Gov't, P.H.S..
Date of Publication 2005 Jul
Year of Publication 2005
Issue/Part 5
Volume 4
Page 324-36
OPIOIDS 2005 <983>
Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)
Unique Identifier 15680308
Status MEDLINE
Authors Sadee W. Wang D. Bilsky EJ.
Authors Full Name Sadee, Wolfgang. Wang, Danxin. Bilsky, Edward J.
Institution
Department of Pharmacology, College of Medicine and Public Health, The Ohio State University, Columbus, OH
43210, USA. sadee.1@osu.sdu
Title
Basal opioid receptor activity, neutral antagonists, and therapeutic opportunities.
[Review] [61 refs]
Source
Life Sciences. 76(13):1427-37, 2005 Feb 11.
Journal Name
Life Sciences
Country of Publication
England
Abstract
The mu opioid receptor (MOR, OPRM)--the principal receptor involved in narcotic addiction-has been shown to display basal (spontaneous, constitutive) signaling activity. Interaction with
other signaling proteins, such as calmodulin, regulates basal MOR activity. Providing a
mechanism for long-lasting regulation, basal MOR activity potentially plays a key role in
addiction, in combination with gene regulation and synaptic remodeling. Recent results
support a link to physical dependence--one of the main manifestations of addiction to drugs of
abuse. The prototypical opioid antagonists, naloxone and naltrexone, were shown to act as
inverse agonists in the morphine-dependent state (i.e., they suppress basal MOR signaling)
and thereby appear to elicit or contribute to precipitated withdrawal. This affords the
opportunity to explore therapeutic applications for neutral antagonists (blocking agonists at
MOR without affecting basal activity) with reduced adverse effects. Neutral antagonists are
promising drug candidates in the treatment of addiction and overdose, and of peripheral
adverse effects of narcotic analgesics. [References: 61]
ISSN Print 0024-3205
Publication Type Journal Article. Research Support, U.S. Gov't, P.H.S.. Review.
Date of Publication 2005 Feb 11
Year of Publication 2005
Issue/Part 13
Volume 76
Page 1427-37