PHARMACOLOGY 2008/ COCAINE 2008 / ALCOHOL 2008 <152>
PHARMACOLOGY 2008/ COCAINE 2008 / ALCOHOL 2008 <152>
Database
EMBASE
Accession Number
2008571958
Authors
Suh J.J. Pettinati H.M. Kampman K.M. O'Brien C.P.
Institution
(Suh, Pettinati, Kampman, O'Brien) Center for Studies of Addiction, Department of Psychiatry, University of Pennsylvania School of Medicine, Philadelphia, PA, United States.
(Suh, Kampman, O'Brien) PhiladelphiaVeteransAffairsMedicalCenter, Philadelphia, PA, United States.
(Suh) Center for Studies of Addiction, Department of Psychiatry, University of Pennsylvania, 3900 Chestnut St, Philadelphia, PA 19104, United States.
Country of Publication
United Kingdom
Title
Gender differences in predictors of treatment attrition with high dose naltrexone in cocaine and alcohol dependence.
Source
American Journal on Addictions. 17(6)(pp 463-468), 2008. Date of Publication: November 2008.
Publisher
Informa Healthcare
Abstract
Recently, we reported that naltrexone at 150 mg/day significantly decreased cocaine and alcohol use for men but not women with co-occurring cocaine and alcohol dependence. The present study is an exploratory investigation of predictors that explain the different gender responses to naltrexone, with a particular focus on differential predictors of treatment attrition. No significant predictors were associated with treatment discontinuation in men. Women, however, were more likely to discontinue treatment when reporting severe pre-treatment psychiatric problems or nausea while in treatment. Further research on the impact of pre-treatment and in-treatment gender differences with naltrexone is warranted. Copyright copyright American Academy of Addiction Psychiatry.
ISSN 1055-0496
Publication Type Journal: Article
Journal Name American Journal on Addictions
Volume 17
Issue Part 6
Page 463-468
Year of Publication 2008
Date of Publication November 2008
COCAINE (A) 2008<198>
Database EMBASE
Accession Number 2008485173
Authors Briand L.A. Flagel S.B. Garcia-Fuster M.J. Watson S.J. Akil H. Sarter M. Robinson T.E.
Institution
(Briand, Watson, Akil, Sarter, Robinson) Neuroscience Program, University of Michigan, Ann Arbor, MI, United States.
(Flagel, Garcia-Fuster, Watson, Akil) Molecular and Behavioral Neuroscience Institute, Ann Arbor, MI, United States.
(Sarter, Robinson) Biopsychology Program, Department of Psychology, University of Michigan, Ann Arbor, MI, United States.
(Robinson) Biopsychology Program, Department of Psychology, University of Michigan, 530 Church St., Ann Arbor, MI 48109, United States.
Country of Publication
United Kingdom
Title
Persistent alterations in cognitive function and prefrontal dopamine D2 receptors following extended, but not limited, access to self-administered cocaine.
Source
Neuropsychopharmacology. 33(12)(pp 2969-2980), 2008. Date of Publication: November 2008.
Publisher
Nature Publishing Group
Abstract
Drug addicts have deficits in frontocortical function and cognition even long after the discontinuation of drug use. It is not clear, however, whether the cognitive deficits are a consequence of drug use, or are present prior to drug use, and thus are a potential predisposing factor for addiction. To determine if self-administration of cocaine is capable of producing long-lasting alterations in cognition, rats were allowed access to cocaine for either 1 h/day (short access, ShA) or 6 h/day (long access, LgA) for 3 weeks. Between 1 and 30 days after the last self-administration session, we examined performance on a cognitively demanding test of sustained attention that requires an intact medial prefrontal cortex. The expression levels of dopamine D1 and D2 receptor mRNA and D2 protein in the prefrontal cortex were also examined. Early after discontinuation of drug use, LgA (but not ShA) animals were markedly impaired on the sustained attention task. Although the LgA animals improved over time, they continued to show a persistent pattern of performance deficits indicative of a disruption of cognitive flexibility up to 30 days after the discontinuation of drug use. This was accompanied by a significant decrease in DA D2 (but not D1) mRNA in the medial and orbital prefrontal cortex, and D2 receptor protein in the medial prefrontal cortex of LgA (but not ShA) animals. These findings establish that repeated cocaine use is capable of producing persistent alterations in the prefrontal cortex and in cognitive function, and illustrate the usefulness of extended access self-administration procedures for studying the neurobiology of addiction. copyright 2008 Nature Publishing Group All rights reserved.
ISSN 0893-133X
Publication Type Journal: Article
Journal Name Neuropsychopharmacology
Volume 33
Issue Part 12
Page 2969-2980
Year of Publication 2008
Date of Publication November 2008
COCAINE (A) 2008<199>
Database EMBASE
Accession Number 2008485170
Authors Schroeder F.A. Penta K.L. Matevossian A. Jones S.R. Konradi C. Tapper A.R. Akbarian S.
Institution
(Schroeder, Penta, Matevossian, Tapper, Akbarian) Department of Psychiatry, Brudnick Neuropsychiatric Research Institute, Worcester, MA, United States.
(Schroeder) Program in Neuroscience, University of MassachusettsGraduateSchool of Biomedical Sciences, Worcester, MA, United States.
(Jones) Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC, United States.
(Konradi) Department of Psychiatry, VanderbiltUniversity, Nashville, TN, United States.
(Akbarian) Department of Psychiatry, University of Massachusetts Medical School, Brudnick Neuropsychiatric Research Institute, 303 Belmont Street, Worcester, MA 01604, United States.
Country of Publication
United Kingdom
Title
Drug-induced activation of dopamine D1 receptor signaling and inhibition of class I/II histone deacetylase induce chromatin remodeling in reward circuitry and modulate cocaine-related behaviors.
Source
Neuropsychopharmacology. 33(12)(pp 2981-2992), 2008. Date of Publication: November 2008.
Publisher
Nature Publishing Group
Abstract
Chromatin remodeling, including histone modification, is involved in stimulant-induced gene expression and addiction behavior. To further explore the role of dopamine D1 receptor signaling, we measured cocaine-related locomotor activity and place preference in mice pretreated for up to 10 days with the D1 agonist SKF82958 and/or the histone deacetylase inhibitor (HDACi), sodium butyrate. Cotreatment with D1 agonist and HDACi significantly enhanced cocaine-induced locomotor activity and place preference, in comparison to single-drug regimens. However, butyrate-mediated reward effects were transient and only apparent within 2 days after the last HDACi treatment. These behavioral changes were associated with histone modification changes in striatum and ventral midbrain: (1) a generalized increase in H3 phosphoacetylation in striatal neurons was dependent on activation of D 1 receptors; (2) H3 deacetylation at promoter sequences of tyrosine hydroxylase (Th) and brain-derived neurotrophic factor (Bdnf) in ventral midbrain, together with upregulation of the corresponding gene transcripts after cotreatment with D1 agonist and HDACi. Collectively, these findings imply that D1 receptor-regulated histone (phospho)acetylation and gene expression in reward circuitry is differentially regulated in a region-specific manner. Given that the combination of D1 agonist and HDACi enhances cocaine-related sensitization and reward, the therapeutic benefits of D1 receptor antagonists and histone acetyl-transferase inhibitors (HATi) warrant further investigation in experimental models of stimulant abuse. copyright 2008 Nature Publishing Group All rights reserved.
ISSN 0893-133X
Publication Type Journal: Article
Journal Name Neuropsychopharmacology
Volume 33
Issue Part 12
Page 2981-2992
Year of Publication 2008
Date of Publication November 2008
COCAINE 2008<214>
Database EMBASE
Accession Number 2008460986
Authors Vlachou S. Stamatopoulou F. Nomikos G.G. Panagis G.
Institution
(Vlachou, Stamatopoulou, Panagis) Department of Psychology, School of Social Sciences, University of Crete, Rethymnon, Crete, Greece.
(Nomikos) Cannasat Therapeutics, Toronto, ON, Canada.
(Panagis) University of Crete, School of Social Sciences, Department of Psychology, 74100 Rethymnon, Crete, Greece.
Country of Publication
United Kingdom
Title
Enhancement of endocannabinoid neurotransmission through CB1 cannabinoid receptors counteracts the reinforcing and psychostimulant effects of cocaine.
Source
International Journal of Neuropsychopharmacology. 11(7)(pp 905-923), 2008. Date of Publication: November 2008.
Publisher
CambridgeUniversity Press
Abstract
Cannabinoids, in contrast to typical drugs of abuse, have been shown to exert complex effects on behavioural reinforcement and psychomotor function. We have shown that cannabinoid agonists lack reinforcing/rewarding properties in the intracranial self-stimulation (ICSS) paradigm and that the CB1 receptor (CB1R) agonist WIN55,212-2 attenuates the reward-facilitating actions of cocaine. We sought to determine the effects of the endocannabinoid neurotransmission enhancer AM-404 (1, 3, 10, 30 mg/kg) on the changes in ICSS threshold and locomotion elicited by cocaine and extend the study of the effects of WIN55,212-2 (0.3, 1, 3 mg/kg) on cocaine-induced hyperlocomotion. AM-404 did not exhibit reward-facilitating properties, and actually increased self-stimulation threshold at the highest dose. Cocaine significantly reduced self-stimulation threshold, without altering maximal rates of responding. AM-404 (10 mg/kg) attenuated this action of cocaine, an effect which was reversed by pretreatment with the selective CB1R antagonist SR141716A. WIN55,212-2 decreased locomotion at the two highest doses, an effect that was blocked by SR141716A; AM-404 had no effect on locomotion. Cocaine caused a significant, dose-dependent increase in locomotion, which was reduced by WIN55,212-2 and AM-404. SR141716A blocked the effects of WIN55,212-2 and AM-404 on cocaine-induced hyperlocomotion. SR141716A alone had no effect on ICSS threshold or locomotion. These results indicate that cannabinoids may interfere with brain reward systems responsible for the expression of acute reinforcing/rewarding properties of cocaine, and provide further evidence that the cannabinoid system could be explored as a potential drug discovery target for the treatment of psychostimulant addiction and pathological states associated with psychomotor overexcitability. Copyright copyright 2008 CINP.
ISSN 1461-1457
Publication Type Journal: Article
Journal Name International Journal of Neuropsychopharmacology
Volume 11
Issue Part 7
Page 905-923
Year of Publication 2008
Date of Publication November 2008
COCAINE 2008<223>
Database EMBASE
Accession Number 2008480093
Authors Chen Q. Xiong X. Lee T.H. Liu Y. Wetsel W.C. Zhang X.
Institution
(Chen, Xiong, Lee, Wetsel, Zhang) Department of Psychiatry and Behavioral Sciences, DukeUniversityMedicalCenter, Durham, NC, United States.
(Liu) Department of Surgery, DukeUniversityMedicalCenter, Durham, NC, United States.
(Wetsel) Department of Cell Biology, DukeUniversityMedicalCenter, Durham, NC, United States.
(Zhang) Department of Psychiatry and Behavioral Science, DukeUniversityMedicalCenter, Box 3870, Durham, NC27710, United States.
Country of Publication
United Kingdom
Title
Neural plasticity and addiction: Integrin-linked kinase and cocaine behavioral sensitization.
Source
Journal of Neurochemistry. 107(3)(pp 679-689), 2008. Date of Publication: November 2008.
Publisher
Blackwell Publishing Ltd
Abstract
Behavioral sensitization of psychostimulants was accompanied by alterations in a variety of biochemical molecules in different brain regions. However, which change is actually related to drug-produced sensitization lacks of accurate clarification. In this study, we investigated the role of integrin-linked kinase (ILK) in both the induction and expression of cocaine sensitization. Conditional inhibition of ILK expression was established in the nucleus accumbens (NAc) core by microinjecting recombinant adeno-associated virus-carrying, tetracycline-on-regulated small interfering RNA which reversed the chronic cocaine-induced psychomotor sensitization, as well as the changes in protein kinase B Ser473 phosphorylation, dendritic density, and dendritic spine numbers locally. Importantly, the reversed psychomotor sensitization did not recover after cessation of the silencing for 8 days. We also demonstrated that inhibition of ILK expression pre- and during-chronic cocaine treatments blocked the induction of cocaine psychomotor sensitization and abolished the stimulant effect of cocaine on ILK expression. In contrast, inhibition of ILK expression in the NAc core has no significant effect on cocaine-induced stereotypical behaviors. This concludes that ILK is involved in cocaine sensitization with the earlier induction and later expression functioning as a kinase to regulate protein kinase B Ser473 phosphorylation and a scaffolding protein to regulate the reorganization of the NAc spine morphology. copyright 2008 The Authors.
ISSN 0022-3042
Publication Type Journal: Article
Journal Name Journal of Neurochemistry
Volume 107
Issue Part 3
Page 679-689
Year of Publication 2008
Date of Publication November 2008
COCAINE (A)<270>
Database EMBASE
Accession Number 2008390017
Authors George O. Mandyam C.D. Wee S. Koob G.F.
Institution
(George, Mandyam, Wee, Koob) Committee on the Neurobiology of Addictive Disorders, Scripps Research Institute, San Diego, CA, United States.
(George) Committee on the Neurobiology of Addictive Disorders, Scripps Research Institute, SP30-2400, 10550 North Torrey Pines Road, San Diego, CA 92037, United States.
Country of Publication
United Kingdom
Title
Extended access to cocaine self-administration produces long-lasting prefrontal cortex-dependent working memory impairments.
Source
Neuropsychopharmacology. 33(10)(pp 2474-2482), 2008. Date of Publication: September 2008.
Publisher
Nature Publishing Group
Abstract
Humans with drug addiction exhibit compulsive drug-seeking associated with impairment of prefrontal cortex cognitive function. Whether prefrontal cortex dysfunction is a consequence of chronic drug exposure, or mediates the transition from drug use to drug dependence, is unknown. The current study investigates whether a history of escalated vs controlled cocaine intake is associated with specific working memory impairments, and long-lasting alterations of the dorsomedial prefrontal cortex and orbitofrontal cortex in rats. Working memory was assessed in rats with a history of extended (6 h per session) or limited (1 h per session) access to cocaine (0.5 mg/kg per injection), 3-17 days after the last self-administration session, using a delayed nonmatching-to-sample task. The density of neurons, oligodendrocytes, and astrocytes was quantified in the dorsomedial prefrontal cortex and orbitofrontal prefrontal cortex 2 months after the last self-administration session. Working memory impairments were observed after a history of chronic and escalated cocaine intake, but not after repeated limited access to cocaine. Moreover, working memory impairments were correlated with a decreased density of neurons and oligodendrocytes but not astrocytes in the dorsomedial prefrontal cortex, and with a decreased density of oligodendrocytes in the orbitofrontal cortex. Considering the role of the prefrontal cortex in goal-directed behavior, the prefrontal cortex dysfunctions observed here may exacerbate the loss of control associated with increased drug use and facilitate the progression to drug addiction. copyright 2008 Nature Publishing Group All rights reserved.
ISSN 0893-133X
Publication Type Journal: Article
Journal Name Neuropsychopharmacology
Volume 33
Issue Part 10
Page 2474-2482
Year of Publication 2008
Date of Publication September 2008
COCAINE 2008<288>
Database EMBASE
Accession Number 2008422570
Authors Fairbairn C.E. Dundon W.D. Xie H. Plebani J.G. Kampman K.M. Lynch K.G.
Institution
(Fairbairn, Dundon, Xie, Plebani, Kampman, Lynch) Department of Psychiatry, University of Pennsylvania School of Medicine, Philadelphia, PA, United States.
(Dundon) University of Pennsylvania Treatment Research Center, 3900 Chestnut St, Philadelphia, PA 19104, United States.
Country of Publication
United Kingdom
Title
Study blinding and correlations between perceived group assignment and outcome in a cocaine pharmacotherapy trial.
Source
American Journal on Addictions. 17(5)(pp 387-391), 2008. Date of Publication: September 2008.
Publisher
Informa Healthcare
Abstract
While much research has suggested that the integrity of the blind is compromised in psychotropic drug trials, little research has been conducted on blinding in substance abuse trials. The current study examines the integrity of the blind in an outpatient pharmacotherapy trial investigating the effectiveness of amantadine and propranolol in treating cocaine addiction. Results suggest that neither nurses (N = 174, kappa = 0.08, p = 0.22) nor participants (N = 163, kappa = 0.09, p = 0.26) could accurately predict treatment assignment. Furthermore, nurses' perceptions of treatment assignment were significantly related to trial completion, medication compliance, and cocaine use - results that may have training implications for medical personnel. Copyright copyright American Academy of Addiction Psychiatry.
ISSN 1055-0496
Publication Type Journal: Article
Journal Name American Journal on Addictions
Volume 17
Issue Part 5
Page 387-391
Year of Publication 2008
Date of Publication September 2008
COCAINE 2008<297>
Database EMBASE
Accession Number 2008384509
Authors Numa R. Kohen R. Poltyrev T. Yaka R.
Institution
(Numa, Poltyrev, Yaka) Department of Pharmacology, School of Pharmacy, Faculty of Medicine, Jerusalem, 91120, Israel.
(Numa, Kohen) Department of Pharmaceutics, School of Pharmacy, Faculty of Medicine, Jerusalem, 91120, Israel.
Country of Publication
United Kingdom
Title
Tempol diminishes cocaine-induced oxidative damage and attenuates the development and expression of behavioral sensitization.
Source
Neuroscience. 155(3)(pp 649-658), 2008. Date of Publication: 26 Aug 2008.
Publisher
Elsevier Ltd
Abstract
A variety of mechanisms has been suggested for cocaine toxicity, including the possibility that cocaine induces an increase in oxidative stress (OS) due to excessive oxidation of dopamine (e.g. dopamine quinine), or by redox cycling of cocaine oxidized metabolites. However, the association between oxidative status in the brain and cocaine induced-behavior is poorly understood. Therefore, we examined the ability of the unique antioxidant tempol to attenuate cocaine-induced oxidative damage and behavioral response. Acute cocaine treatment significantly elevated OS markers in prefrontal cortex (PFC) and nucleus accumbens (NAc) in rats, both in slices and following a single cocaine injection, which corresponded with a decrease in total antioxidant capacity (TAC). Tempol, at the optimal concentration we determined that was needed to observe an antioxidant non-toxic effect in vitro (1 mM) and in vivo (200 mg/kg), completely abolished the elevation of OS markers and prevented the reduction in TAC in these areas. Importantly, tempol injections, at a dose that does not affect the basal levels of locomotor activity, attenuated both the development and expression of cocaine-induced locomotor sensitization. Finally, in cocaine-sensitized animals, tempol prevented the elevation of OS markers in both PFC and NAc. Our findings suggest that oxidation of specific sites in the brain reward system by cocaine is accompanied with behavioral changes. Tempol has a neuro-protective effect against cocaine toxicity in these regions, and it may be beneficial in the treatment of cocaine addiction. copyright 2008 IBRO.
ISSN 0306-4522
Publication Type Journal: Article
Journal Name Neuroscience
Volume 155
Issue Part 3
Page 649-658
Year of Publication 2008
Date of Publication 26 Aug 2008
COCAINE (A)<311>
Database EMBASE
Accession Number 2008384003
Authors Bailey A. Metaxas A. Yoo J.H. McGee T. Kitchen I.
Institution
(Bailey, Metaxas, Yoo, McGee, Kitchen) Faculty of Health and Medical Sciences, AY Building, University of Surrey, Guildford, SurreyGU2 7XH, United Kingdom.
Country of Publication
United Kingdom
Title
Decrease of D2 receptor binding but increase in D 2-stimulated G-protein activation, dopamine transporter binding and behavioural sensitization in brains of mice treated with a chronic escalating dose 'binge' cocaine administration paradigm.
Source
European Journal of Neuroscience. 28(4)(pp 759-770), 2008. Date of Publication: August 2008.
Publisher
Blackwell Publishing Ltd
Abstract
Understanding the neurobiology of the transition from initial drug use to excessive drug use has been a challenge in drug addiction. We examined the effect of chronic 'binge' escalating dose cocaine administration, which mimics human compulsive drug use, on behavioural responses and the dopaminergic system of mice and compared it with a chronic steady dose (3 x 15 mg/;kg/;day) 'binge' cocaine administration paradigm. Male C57BL/;6J mice were injected with saline or cocaine in an escalating dose paradigm for 14 days. Locomotor and stereotypy activity were measured and quantitative autoradiographic mapping of D1 and D2 receptors, dopamine transporters and D 2-stimulated [35S]GTPgammaS binding was performed in the brains of mice treated with this escalating and steady dose paradigm. An initial sensitization to the locomotor effects of cocaine followed by a dose-dependent increase in the duration of the locomotor effect of cocaine was observed in the escalating but not the steady dose paradigm. Sensitization to the stereotypy effect of cocaine and an increase in cocaine-induced stereotypy score was observed from 3 x 20 to 3 x 25 mg/;kg/;day cocaine. There was a significant decrease in D2 receptor density, but an increase in D2-stimulated G-protein activity and dopamine transporter density in the striatum of cocaine-treated mice, which was not observed in our steady dose paradigm. Our results document that chronic 'binge' escalating dose cocaine treatment triggers profound behavioural and neurochemical changes in the dopaminergic system, which might underlie the transition from drug use to compulsive drug use associated with addiction, which is a process of escalation. copyright The Authors (2008).