OPIOIDS 2009 <581>
Database EMBASE
Accession Number 2009441356
Authors Rothwell P.E. Thomas M.J. Gewirtz J.C.
Institution
(Rothwell, Thomas, Gewirtz) Graduate Program in Neuroscience, Departments of Neuroscience and Psychology, University of Minnesota, Minneapolis, MN, United States.
(Gewirtz) Psychology and Neuroscience, University of Minnesota, 75 East River Road, Minneapolis, MN 55455, United States.
Country of Publication
United Kingdom
Title
Distinct profiles of anxiety and dysphoria during spontaneous withdrawal from acute morphine exposure.
Source
Neuropsychopharmacology. 34(10)(pp 2285-2295), 2009. Date of Publication: September 2009.
Publisher
Nature Publishing Group
Abstract
The negative motivational aspects of withdrawal include symptoms of both anxiety and depression, and emerge after termination of chronic drug use as well as after acute drug exposure. States of acute withdrawal are an inherent part of intermittent drug use in humans, but the contribution of acute withdrawal to the development of addiction has received limited systematic investigation, because of a lack of preclinical models for withdrawal states that emerge spontaneously after acute drug exposure. Here, we have characterized a spontaneous increase in the magnitude of the acoustic startle reflex (ie, spontaneous withdrawal-potentiated startle) that emerges after acute morphine administration in rats, and compared the time course of startle potentiation and place conditioning. We find that startle potentiation seems to be related to a decrease in opiate receptor occupancy and reflects an anxiety-like state with a pharmacological profile similar to other signs of opiate withdrawal. Spontaneous startle potentiation emerges before the rewarding effects of morphine have subsided, even though naloxone administration after a single morphine exposure causes both startle potentiation and conditioned place aversion (CPA). These results show that negative emotional signs of withdrawal develop after just one exposure to morphine, and are likely a recurrent aspect of intermittent drug use that may contribute to the earliest adaptations underlying the development of addiction. Furthermore, the dissociation between spontaneous startle potentiation and CPA suggests anxiogenic and dysphoric manifestations of opiate withdrawal may be mediated by distinct neural mechanisms that are progressively engaged as withdrawal unfolds. copyright 2009 Nature Publishing Group All rights reserved.
ISSN 0893-133X
Publication Type Journal: Article
Journal Name Neuropsychopharmacology
Volume 34
Issue Part 10
Page 2285-2295
Year of Publication 2009
Date of Publication September 2009
OPIOIDS (A) 2009 <589>
DatabaseEMBASE
Accession Number 2009496590
Authors Bilecki W. Wawrzczak-Bargiela A. Przewlocki R.
Institution
(Bilecki, Wawrzczak-Bargiela, Przewlocki) Molecular Neuropharmacology, Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna Street, 31343 Krakow, Poland.
Country of Publication
United Kingdom
Title
Regulation of kinesin light chain 1 level correlates with the development of morphine reward in the mouse brain.
Source
European Journal of Neuroscience. 30(6)(pp 1101-1110), 2009. Date of Publication: September 2009.
Publisher
Blackwell Publishing Ltd
Abstract
Persistent changes that take place during the development of opioid addiction are thought to be due to reorganization of synaptic connections in relevant brain circuits. This neuronal plasticity requires trafficking of signaling molecules that are controlled by kinesins. In neurons, kinesin light chain 1 (KLC1) acts as the primary regulator of kinesin action. We observed that KLC1 was enriched in sub-cortical regions of the brain in C57Bl/6J mice. KLC1 expression was especially enriched in the striatum, hippocampus and amygdala, which are known to be involved in opioid addiction. Our study revealed that conditioning of C57Bl/6J mice with morphine elevated KLC1 levels in the amygdala, frontal cortex and hippocampus, but not in the striatum. Further study revealed that alterations in KLC1 protein levels in the studied brain regions correlated with the expression of morphine-induced conditioned place preference. In the cortex, hippocampus and amygdala, KLC1 co-localized with calcium/calmodulin-dependent protein kinase II (CaMKII), suggesting that KLC1 was present in the cell bodies and dendrites of pyramidal neurons. Our findings indicate that KLC1, a molecule involved in dendritic and axonal transport in the brain, is affected during chronic morphine treatment and may be involved in the development of opioid addiction. copyright Federation of European Neuroscience Societies and Blackwell Publishing Ltd.
ISSN 0953-816X
Publication Type Journal: Article
Journal Name European Journal of Neuroscience
Volume 30
Issue Part 6
Page 1101-1110
Year of Publication 2009
Date of Publication September 2009
OPIOIDS 2009 <592>
Database EMBASE
Accession Number 2009480348
Authors Gowing L. Ali R. White J.M.
Institution
(Gowing, Ali, White) Discipline of Pharmacology, University of Adelaide, Frome Road, Adelaide, SA 5005, Australia.
Country of Publication
United Kingdom
Title
Buprenorphine for the management of opioid withdrawal.
Source
Cochrane Database of Systematic Reviews. (3), 2009. Article Number: CD002025. Date of Publication: 2009.
Publisher
John Wiley and Sons Ltd
Abstract
Background: Managed withdrawal is a necessary step prior to drug-free treatment or as the end point of substitution treatment. Objectives: To assess the effectiveness of interventions involving the use of buprenorphine to manage opioid withdrawal, for withdrawal signs and symptoms, completion of withdrawal and adverse effects. Search strategy: We searched the Cochrane Central Register of Controlled Trials (The Cochrane Library, Issue 3, 2008), MEDLINE (January 1966 to July 2008), EMBASE (January 1985 to 2008 Week 31), PsycINFO (1967 to 7 August 2008) and reference lists of articles. Selection criteria: Randomised controlled trials of interventions involving the use of buprenorphine to modify the signs and symptoms of withdrawal in participants who were primarily opioid dependent. Comparison interventions involved reducing doses ofmethadone, alpha2-adrenergic agonists, symptomatic medications or placebo, or different buprenorphine-based regimes. Data collection and analysis: One author assessed studies for inclusion and methodological quality, and undertook data extraction. Inclusion decisions and the overall process was confirmed by consultation between all authors. Main results: Twenty-two studies involving 1736 participants were included. The major comparisons were with methadone (5 studies) and clonidine or lofexidine (12 studies). Five studies compared different rates of buprenorphine dose reduction. Severity of withdrawal is similar for withdrawal managed with buprenorphine and withdrawal managed with methadone, but withdrawal symptoms may resolve more quickly with buprenorphine. It appears that completion of withdrawal treatment may be more likely with buprenorphine relative to methadone (RR 1.18; 95% CI 0.93 to 1.49, P = 0.18) but more studies are required to confirm this. Relative to clonidine or lofexidine, buprenorphine is more effective in ameliorating the symptoms of withdrawal, patients treated with buprenorphine stay in treatment for longer (SMD 0.92, 95% CI 0.57 to 1.27, P < 0.001), and are more likely to complete withdrawal treatment (RR 1.64; 95% CI 1.31 to 2.06, P < 0.001). At the same time there is no significant difference in the incidence of adverse effects, but drop-out due to adverse effects may be more likely with clonidine. Authors' conclusions: Buprenorphine is more effective than clonidine or lofexidine for themanagement of opioid withdrawal. Buprenorphine may offer some advantages over methadone, at least in inpatient settings, in terms of quicker resolution of withdrawal symptoms and possibly slightly higher rates of completion of withdrawal. Copyright copyright 2009 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd.
ISSN 1469-493X
Publication Type Journal: Review
Journal Name Cochrane Database of Systematic Reviews
Issue Part 3
Year of Publication 2009
Date of Publication 2009
OPIOIDS 2009 <596>
Database EMBASE
Accession Number 2009498153
Authors Carson H.J. Feickert B.L.
Institution
(Carson) Linn County Medical Examiner's Office, Cedar Rapids, IA, United States.
(Feickert) Marion Police Department, Marion, IA, United States.
Country of Publication
United Kingdom
Title
Identification at autopsy of pulverized pills in lungs of a first-time methadone user.
Source
Journal of Forensic and Legal Medicine. 16(8)(pp 494-496), 2009. Date of Publication: November 2009.
Publisher
Churchill Livingstone
Abstract
We recently encountered a 25-year-old white man who died of substance abuse including methadone. The route of administration of the drug(s) appears to have been insufflation. He was found dead at home. There were bottles of prescribed medications and an empty bottle of non-prescribed methadone. There was a grinding device nearby. At autopsy, no needle tracts were identified. Microscopically, the bronchi had desquamated ciliated respiratory epithelium admixed with red-brown pigment, which was found under plane-polarized light to be comprised of birefringent finely-granular material consistent with pulverized pills. Blood toxicology was positive for tetrahydrocannabinol, sertraline, nicotine, and methadone. The cause of death was ruled drug interactions with cerebral and pulmonary edema, the manner of death accidental. The decedent fit a profile of a victim of prescription drug abuse, for whom the mode of administration of drugs may be altered from intended use in as many as 80% of cases. copyright 2009 Elsevier Ltd and Faculty of Forensic and Legal Medicine.
ISSN 1752-928X
Publication Type Journal: Article
Journal Name Journal of Forensic and Legal Medicine
Volume 16
Issue Part 8
Page 494-496
Year of Publication 2009
Date of Publication November 2009
OPIOIDS 2009 <606>
Database EMBASE
Accession Number 2009509589
Authors Mammen K. Bell J.
Institution
(Mammen) Langton Centre, South Eastern Sydney and Illawarra Area Health Service, 591 South Dowling Street, Surry Hills, NSW 2010, Australia.
(Bell) South London and Maudsley NHS Foundation Trust, Marina House, 65 Denmark Hill, London SE5 8RS, United Kingdom.
Country of Publication
United Kingdom
Title
The clinical efficacy and abuse potential of combination buprenorphine-naloxone in the treatment of opioid dependence.
Source
Expert Opinion on Pharmacotherapy. 10(15)(pp 2537-2544), 2009. Date of Publication: October 2009.
Publisher
Informa Healthcare
Abstract
Background: Opioid dependence is a chronic relapsing condition for which long-term opioid substitution treatment (OST) is effective. However, safety and community acceptance of OST is compromised by diversion of prescribed medication. The development of a formulation combining buprenorphine and naloxone is designed to reduce the likelihood of intravenous misuse, and the therefore the value of the medication if diverted to the black market. Objective: To evaluate the evidence for 4:1 buprenorphine-naloxone as an efficacious OST, and as a deterrent to diversion and intravenous misuse. Methods: The literature on buprenorphine-naloxone in a 4:1 ratio is reviewed. Results/conclusion: The addition of naloxone does not appear to affect the efficacy of buprenorphine as a maintenance drug. While offering some deterrence of injection through precipitated withdrawal, there are many circumstances where injecting of buprenorphine-naloxone is reinforcing rather than aversive. The combination will reduce, but not eliminate, intravenous misuse; clinicians therefore need to monitor patients in OST, and be selective in providing patients with medication to be taken without observation. copyright 2009 Informa UK Ltd. All rights reserved.
ISSN 1465-6566
Publication Type Journal: Review
Journal Name Expert Opinion on Pharmacotherapy
Volume 10
Issue Part 15
Page 2537-2544
Year of Publication 2009
Date of Publication October 2009
OPIOIDS 2009 <623>
Database EMBASE
Accession Number 2009495842
Authors Doehring A. Hentig N.V. Graff J. Salamat S. Schmidt M. Geisslinger G. Harder S. Lotsch J.
Institution
(Doehring, Hentig, Graff, Salamat, Geisslinger, Harder, Lotsch) Pharmazentrum Frankfurt/ZAFES, Institute of Clinical Pharmacology, Goethe-University, Theodor Stern Kai 7, D-60590 Frankfurt am Main, Germany.
(Schmidt) Malteser Drogenambulanz Schielestrasse, Schielestrasse, Frankfurt am Main, Germany.
Country of Publication
United Kingdom
Title
Genetic variants altering dopamine D2 receptor expression or function modulate the risk of opiate addiction and the dosage requirements of methadone substitution.
Source
Pharmacogenetics and Genomics. 19(6)(pp 407-414), 2009. Date of Publication: 01 Jun 2009.
Publisher
Lippincott Williams and Wilkins
Abstract
AIM: Addictive behavior is importantly mediated by mesolimbic dopaminergic signaling. Here, we comprehensively analyzed the DRD2 gene locus, and in addition, the ANKK1 rs1800497C>T single nucleotide polymorphism (SNP), formerly known as 'dopamine D2 receptor Taq1A C>T polymorphism, for associations with the risk of opiate addiction and the methadone dosage requirements. METHODS: Allelic frequencies of DRD2/ANKK1 polymorphisms were compared between 85 methadone-substituted Caucasian patients and a random sample of 99 healthy Caucasian controls. Within patients, the average and maximum daily methadone dose during the first year of treatment and the time when that maximum dose was reached were analyzed for an association with DRD2/ANKK1 genetics. RESULTS: Compared with the control group, drug users carried more frequently the minor allele of DRD2 SNP rs1076560G>T SNP (P=0.022, odds ratio 2.343) or the ATCT haplotype of DRD2 rs1799978A>G, rs1076560G>T, rs6277C>T, ANKK1 rs1800497C>T (P=0.048, odds ratio 2.23), with similar tendencies for ANKK1 rs1800497C>T (P=0.056, odds ratio 2.12) and the TCCTCTT haplotype of DRD2 rs12364283T>C, rs1799732C del, rs4648317C>T, rs1076560G>T, rs6275C>T, rs6277C>T, and ANKK1 rs1800497C>T (P=0.059, odds ratio 2.31). The average and maximum daily methadone doses were significantly associated with the DRD2 rs6275C>T SNP (P=0.016 and 0.005 for average and maximum dose, respectively). Carriers of the variant rs6275T allele needed higher methadone doses than noncarriers. In addition, this variant was associated with a longer time to reach the maximum methadone dose (P=0.025). CONCLUSION: On the basis of an analysis spanning the whole gene locus, from the DRD2 promoter to the ANKK1 rs1800497C>T polymorphism, DRD2 genetic polymorphisms modulate both the risk of opiate addiction, leading to the necessity of methadone substitution therapy, and the course of this therapy in terms of dosage requirements. copyright 2009 Wolters Kluwer Health.
ISSN 1744-6872
Publication Type Journal: Article
Journal Name Pharmacogenetics and Genomics
Volume 19
Issue Part 6
Page 407-414
Year of Publication 2009
Date of Publication 01 Jun 2009
OPIOIDS 2009 <631>
Database EMBASE
Accession Number 2009525082
Authors Hofford R.S. Hodgson S.R. Roberts K.W. Bryant C.D. Evans C.J. Eitan S.
Institution
(Hofford, Hodgson, Eitan) Department of Psychology, Behavioral and Cellular Neuroscience, Texas A and M University, College Station, TX, United States.
(Roberts, Evans) Department of Psychiatry and Biobehavioral Sciences, UCLA, Neuropsychiatric Institute, Westwood Plaza, Los Angeles, CA, United States.
(Bryant) Department of Human Genetics, University of Chicago, CLSC, Chicago, IL, United States.
(Eitan) Texas A and M University, Department of Psychology, 4235 TAMU, College Station, TX 77843, United States.
Country of Publication
United Kingdom
Title
Extracellular signal-regulated kinase activation in the amygdala mediates elevated plus maze behavior during opioid withdrawal.
Source
Behavioural Pharmacology. 20(7)(pp 576-583), 2009. Date of Publication: October 2009.