COCAINE 2007 / AMPHETAMINES 2007 <483>
Database EMBASE
Accession Number 2008280167
Authors Knapp W.P. Soares B. Farrel M. Lima M.S.
Institution
(Knapp) Psychology, PUC, RS, Avenue Paulo Gama 110, Porto Alegre, Brazil.
Country of Publication
United Kingdom
Title
Psychosocial interventions for cocaine and psychostimulant amphetamines related
disorders.
Source
Cochrane Database of Systematic Reviews. (3), 2007. Article Number: CD003023. Date of
Publication: 2007.
Abstract
Background: The consumption of psychostimulants for non-medical reasons probably occurs
because of their euphoriant and psychomotor-stimulating properties. Chronic consumption of
these agents results in development of stereotyped behaviour, paranoia, and possibly
aggressive behaviour. Psychosocial treatments for psychostimulant use disorder are
supposed to improve compliance, and to promote abstinence. Evidence from randomised
controlled trials in this subject needs to be summarised. Objectives: To conduct a systematic
review of all RCTs on psychosocial interventions for treating psychostimulant use disorder.
Search strategy: Electronic searches of Cochrane Library, EMBASE, MEDLINE, and LILACS
(to may 2006); reference searching; personal communication; conference abstracts;
unpublished trials from pharmaceutical industry; book chapters on treatment of
psychostimulants abuse/dependence. Selection criteria: All randomised-controlled trials
focusing on psychosocial interventions for treating psychostimulants abuse/ dependence.
Data collection and analysis: Three authors extracted the data independently and Relative
Risks, weighted mean difference and number needed to treat were estimated, when possible.
The reviewers assumed that people who died or dropped out had no improvement (intention
to treat analysis) and tested the sensitivity of the final results to this assumption. Main results:
Twenty-seven randomised controlled studies (3663 participants) fulfilled inclusion criteria and
had data that could be used for at least one of the main comparisons. There was a wide
heterogeneity in the interventions evaluated: this did not allow to provide a summary estimate
of effect and results cannot be summarised in a clear cut way. The comparisons between
different type of Behavioural Interventions showed results in favour of treatments with some
form of Contingency management in respect to both reducing drop outs and lowering cocaine
use. Authors' conclusions: Overall this review reports little significant behavioural changes
with reductions in rates of drug consumption following an intervention. Moreover, with the
evidence currently available, there are no data supporting a single treatment approach that is
able to comprise the multidimensional facets of addiction patterns and to significantly yield
better outcomes to resolve the chronic, relapsing nature of addiction, with all its correlates
and consequences. Copyright copyright 2008 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 2007
Date of Publication 2007
COCAINE 2007 <486>
Database EMBASE
Accession Number 2008279981
Authors Amato L. Minozzi S. Pani P.P. Davoli M.
Institution
(Amato) Deparment of Epidemiology, ASL RM/E, Via di Santa Costanza 53, Rome Lazio 00198, Italy.
Country of Publication
United Kingdom
Title
Antipsychotic medications for cocaine dependence.
Source
Cochrane Database of Systematic Reviews. (3), 2007. Article Number: CD006306. Date of
Publication: 2007.
Abstract
Background: Cocaine dependence is a public health problem characterized by recidivism
and a host of medical and psychosocial complications. Cocaine dependence remains a
disorder for which no pharmacological treatment of proven efficacy exists, although
considerable advances in the neurobiology of this addiction could guide future medication
development. Objectives: To evaluate the efficacy and the acceptability of antipsychotic
medications for cocaine dependence. Search strategy: We searched the following sources:
MEDLINE (1966 to October 2006), EMBASE (1980 to October 2006), CINAHL (1982 to
October 2006), Cochrane Drug and Alcohol Group Specialised Register (October 2006). We
also searched the reference lists of trials, the main electronic sources of ongoing trials
(National Research Register, meta-Register of Controlled Trials; Clinical Trials.gov) and
conference proceedings likely to contain trials relevant to the review. All searches included
also non-English language literature. Selection criteria: All randomised controlled trials and
controlled clinical trials with focus on the use of any antipsychotic medication for cocaine
dependence. Data collection and analysis: Two authors independently evaluated the papers,
extracted data, rated methodological quality. Main results: Seven small studies were included
(293 participants): the antipsychotic drugs studied were risperidone, olanzapine and
haloperidol. No significant differences were found for any of the efficacy measures comparing
any antipsychotic with placebo. Risperidone was found to be superior to placebo in
diminishing the number of dropouts, four studies, 178 participants, Relative Risk (RR) 0.77
(95%CI 0.77 to 0.98). Most of the included studies did not report useful results on important
outcomes such as side effects, use of cocaine during treatment and craving. The results on
olanzapine and haloperidol come from studies too small to give conclusive results. Authors'
conclusions: Although caution is needed when assessing results from a limited number of
small clinical trials there is no current evidence, at the present, supporting the clinical use of
antipsychotic medications in the treatment of cocaine dependence. Furthermore, most of the
included studies did not report useful results on important outcomes such as side effects, use
of cocaine during the treatment and craving. Aiming to answer the urgent demand of
clinicians, patients, families, and the community as a whole for an adequate treatment for
cocaine dependence, larger randomised investigations should be designed investigating
relevant outcomes and reporting data to allow comparison of results between studies.
Moreover some efforts should be done also to investigate the efficacy of other type
medications, like anticonvulsant, currently used in clinical practice. Copyright copyright 2008
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 2007
Date of Publication 2007
COCAINE (A) 2007 <618>
Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)
Unique Identifier 17298672
Status PubMed-not-MEDLINE
Authors Pamplona FA. Vendruscolo LF. Takahashi RN.
Authors Full Name Pamplona, Fabricio A. Vendruscolo, Leandro F. Takahashi, Reinaldo N.
Institution
Departamento de Farmacologia, Centro de Ciencias Biologicas, Universidade Federal de Santa Catarina,
Florianopolis, SC, Brazil. fabriciopamplona@uol.com.br
Title
Increased sensitivity to cocaine-induced analgesia in Spontaneously Hypertensive
Rats (SHR).
Source
Behavioral & Brain Functions [Electronic Resource]: BBF. 3:9, 2007.
Journal Name
Behavioral & Brain Functions [Electronic Resource]: BBF
Other ID
Source: NLM. PMC1802084
Country of Publication
England
Abstract
This study examined the analgesic effect of cocaine in Spontaneously Hypertensive Rats
(SHR), which are considered a suitable model for the study of attention deficit hyperactivity
disorder (ADHD), and in Wistar (WIS) rats of both sexes using the hot-plate test. In addition,
we tested whether habituation to the unheated hot-plate apparatus, that "normalizes" the
basal hypoalgesic phenotype of SHR, alters the subsequent cocaine-induced analgesia (CIA)
in this strain. SHR of both sexes were hypoalgesic compared to WIS rats in the hot-plate test
and showed higher sensitivity to CIA. Habituation to the unheated hot-plate reduced the basal
nociceptive latency of SHR, suggesting cognitive/emotional modulation of pain in this strain,
but did not alter the magnitude of CIA. The present study shows increased sensitivity to CIA
in SHR, which may be related to abnormalities in the mesocorticolimbic dopaminergic system.
Further studies using SHR strain may reveal new information on the neurobiological
mechanisms underlying ADHD and its co-morbidity with drug addiction.
Publication Type Journal Article.
Date of Publication 2007
Year of Publication 2007
Volume 3
Page 9
COCAINE (A) 2007 <812>
Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)
Unique Identifier 17900777
Status MEDLINE
Authors Porrino LJ. Smith HR. Nader MA. Beveridge TJ.
Authors Full Name Porrino, Linda J. Smith, Hilary R. Nader, Michael A. Beveridge, Thomas J R.
Institution
Center for the Neurobiological Investigation of Drug Abuse, Department of Physiology and Pharmacology, Wake
Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1083, USA.
lporrino@wfubmc.edu
Title
The effects of cocaine: a shifting target over the course of addiction. [Review] [64 refs]
Source
Progress in Neuro-Psychopharmacology & Biological Psychiatry. 31(8):1593-600, 2007 Nov
15.
Journal Name
Progress in Neuro-Psychopharmacology & Biological Psychiatry
Other ID
Source: NLM. NIHMS34509
Source: NLM. PMC2211431
Country of Publication
England
Abstract
Repeated exposure to psychostimulant drugs such as cocaine has been shown in numerous
studies to produce significant neuroadaptations in both structure and function throughout the
brain. Nonhuman primate models provide a way to systematically evaluate these adaptations
engendered by cocaine self-administration and simulate the progressive nature of cocaine
addiction in humans. Functional activity, measured using the 2-[14C]deoxyglucose method,
was evaluated at selected critical time points over the course of chronic cocaine selfadministration in rhesus monkeys. The effects of cocaine exposure in the initial stages of selfadministration resulted in changes in functional activity in a highly restricted network of
interconnected brain regions when compared to activity in food-reinforced controls. This
pattern of changes was confined mainly to ventromedial prefrontal cortex and ventral striatum.
Following chronic exposure to cocaine self-administration, however, the spatial extent and
intensity of significant alterations in functional activity expanded considerably. The shift in
topography of these changes was orderly, originating ventromedially in the prefrontal corticalventral striatal network and expanding dorsally to encompass the dorsal striatum. A strikingly
similar progression occurred within the cortical areas that project to each of these striatal
regions. Preliminary studies suggest that this pattern is maintained despite periods of
abstinence from cocaine. The shifting patterns of cerebral metabolic function that accompany
longer durations of cocaine self-administration may underlie many of the characteristics of
chronic drug exposure, and may provide transitional mechanisms to more compulsive cocaine
use. [References: 64]
ISSN Print 0278-5846
Publication Type Journal Article. Research Support, N.I.H., Extramural. Review.
Date of Publication 2007 Nov 15
Year of Publication 2007
Issue/Part 8
Volume 31
Page 1593-600
COCAINE (A) 2007 <815>
Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)
Unique Identifier 17888555
Status MEDLINE
Authors Roberts DC. Morgan D. Liu Y.
Authors Full Name Roberts, David C S. Morgan, Drake. Liu, Yu.
Institution
Wake Forest University Health Sciences, Department of Physiology and Pharmacology, Winston-Salem, NC 27157,
United States. dcsrobts@wfubmc.edu
Title
How to make a rat addicted to cocaine. [Review] [78 refs]
Source
Progress in Neuro-Psychopharmacology & Biological Psychiatry. 31(8):1614-24, 2007 Nov
15.
Journal Name
Progress in Neuro-Psychopharmacology & Biological Psychiatry
Other ID
Source: NLM. NIHMS35149
Source: NLM. PMC2140146
Country of Publication
England
Abstract
Procedures have been developed which provide extremely stable patterns of cocaine selfadministration in rats and these have been useful in lesion and drug pretreatment studies
aimed at understanding the neurobiology of cocaine reinforcement. The issue now is whether
studying the neurobiology of reinforcement is the same as studying the neurobiology of
addiction. If the goal is to understand a progressive and deteriorating disorder, then the selfadministration procedures should model specific aspects of the progressive stages of the
addiction process. Here we review theoretical strategies for modeling the addiction process
and present data from a series of experiments from our laboratory showing conditions which
produce a progressive change in the motivation to self-administer cocaine in rats. This
phenomenon is revealed by an escalation in breakpoints on a progressive ratio schedule. The
effect, which is robust and persistent, depends on dose and speed of injection. Interestingly,
high drug intake can retard the development of this effect, which we argue indicates that the
addiction process has a developmental sequence. Finally, we suggest that specific
parameters (dose, price and availability) can be used to examine the transition from
recreational use to binge-like intake. [References: 78]
ISSN Print 0278-5846
Publication Type Journal Article. Research Support, N.I.H., Extramural. Review.
Date of Publication 2007 Nov 15
Year of Publication 2007
Issue/Part 8
Volume 31
Page 1614-24
COCAINE 2007 <834>
Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)
Unique Identifier 17636840
Status MEDLINE
Authors Amato L. Minozzi S. Pani PP. Davoli M.
Authors Full Name Amato, L. Minozzi, S. Pani, P P. Davoli, M.
Institution
ASL RM/E, Deparment of Epidemiology, Via di Santa Costanza 53, Rome, Lazio, Italy, 00198. amato@asplazio.it
Title
Antipsychotic medications for cocaine dependence. [Review] [74 refs]
Source
Cochrane Database of Systematic Reviews. (3):CD006306, 2007.
Journal Name
Cochrane Database of Systematic Reviews
Country of Publication
England
Abstract
BACKGROUND: Cocaine dependence is a public health problem characterized by
recidivism and a host of medical and psychosocial complications. Cocaine dependence
remains a disorder for which no pharmacological treatment of proven efficacy exists, although
considerable advances in the neurobiology of this addiction could guide future medication
development OBJECTIVES: To evaluate the efficacy and the acceptability of antipsychotic
medications for cocaine dependence SEARCH STRATEGY: We searched the following
sources: MEDLINE (1966 to October 2006), EMBASE (1980 to October 2006), CINAHL (1982
to October 2006), Cochrane Drug and Alcohol Group Specialised Register (October 2006).
We also searched the reference lists of trials, the main electronic sources of ongoing trials
(National Research Register, meta-Register of Controlled Trials; Clinical Trials.gov) and
conference proceedings likely to contain trials relevant to the review. All searches included
also non-English language literature. SELECTION CRITERIA: All randomised controlled trials
and controlled clinical trials with focus on the use of any antipsychotic medication for cocaine
dependence DATA COLLECTION AND ANALYSIS: Two authors independently evaluated the
papers, extracted data, rated methodological quality MAIN RESULTS: Seven small studies
were included (293 participants): the antipsychotic drugs studied were risperidone, olanzapine
and haloperidol. No significant differences were found for any of the efficacy measures
comparing any antipsychotic with placebo. Risperidone was found to be superior to placebo in
diminishing the number of dropouts, four studies, 178 participants, Relative Risk (RR) 0.77
(95% CI 0.77 to 0.98). Most of the included studies did not report useful results on important
outcomes such as side effects, use of cocaine during treatment and craving. The results on
olanzapine and haloperidol come from studies too small to give conclusive results.
AUTHORS' CONCLUSIONS: Although caution is needed when assessing results from a
limited number of small clinical trials there is no current evidence, at the present , supporting
the clinical use of antipsychotic medications in the treatment of cocaine dependence.
Furthermore, most of the included studies did not report useful results on important outcomes
such as side effects, use of cocaine during the treatment and craving. Aiming to answer the
urgent demand of clinicians, patients, families, and the community as a whole for an adequate
treatment for cocaine dependence, larger randomised investigations should be designed
investigating relevant outcomes and reporting data to allow comparison of results between
studies. Moreover some efforts should be done also to investigate the efficacy of other type
medications, like anticonvulsant, currently used in clinical practice. [References: 74]
Publication Type Journal Article. Meta-Analysis. Review.
Date of Publication 2007
Year of Publication 2007
Issue/Part 3
Page CD006306
COCAINE / AMPHETAMINES 2007 <836>
Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)
Unique Identifier 17636713
Status MEDLINE
Authors Knapp WP. Soares BG. Farrel M. Lima MS.
Authors Full Name
Knapp, W P. Soares, B G O. Farrel, M. Lima, M S.
Institution
Universidade Federal do Rio Grande do Sul, Psychiatry, Avenue Paulo Gama 110, Porto Alegre, Brazil.
pknapp@terra.com.br
Title
Psychosocial interventions for cocaine and psychostimulant amphetamines related
disorders. [Review] [68 refs]
Source
Cochrane Database of Systematic Reviews. (3):CD003023, 2007.
Journal Name
Cochrane Database of Systematic Reviews
Country of Publication
England
Abstract
BACKGROUND: The consumption of psychostimulants for non-medical reasons probably
occurs because of their euphoriant and psychomotor-stimulating properties. Chronic
consumption of these agents results in development of stereotyped behaviour, paranoia, and
possibly aggressive behaviour. Psychosocial treatments for psychostimulant use disorder are
supposed to improve compliance, and to promote abstinence. Evidence from randomised
controlled trials in this subject needs to be summarised. OBJECTIVES: To conduct a
systematic review of all RCTs on psychosocial interventions for treating psychostimulant use
disorder. SEARCH STRATEGY: Electronic searches of Cochrane Library, EMBASE,
MEDLINE, and LILACS (to may 2006); reference searching; personal communication;
conference abstracts; unpublished trials from pharmaceutical industry; book chapters on
treatment of psychostimulants abuse/ dependence. SELECTION CRITERIA: All randomisedcontrolled trials focusing on psychosocial interventions for treating psychostimulants abuse/
dependence. DATA COLLECTION AND ANALYSIS: Three authors extracted the data
independently and Relative Risks, weighted mean difference and number needed to treat
were estimated, when possible. The reviewers assumed that people who died or dropped out
had no improvement (intention to treat analysis) and tested the sensitivity of the final results
to this assumption. MAIN RESULTS: Twenty-seven randomised controlled studies (3663
participants) fulfilled inclusion criteria and had data that could be used for at least one of the
main comparisons. There was a wide heterogeneity in the interventions evaluated: this did not
allow to provide a summary estimate of effect and results cannot be summarised in a clear
cut way. The comparisons between different type of Behavioural Interventions showed results
in favour of treatments with some form of Contingency management in respect to both
reducing drop outs and lowering cocaine use.. AUTHORS' CONCLUSIONS: Overall this
review reports little significant behavioural changes with reductions in rates of drug
consumption following an intervention. Moreover, with the evidence currently available, there
are no data supporting a single treatment approach that is able to comprise the
multidimensional facets of addiction patterns and to significantly yield better outcomes to
resolve the chronic, relapsing nature of addiction, with all its correlates and consequences.
[References: 68]
Publication Type Journal Article. Review.
Date of Publication 2007
Year of Publication 2007
Issue/Part 3
Page CD003023
COCAINE (A) 2007 <865>
Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)
Unique Identifier 17059838
Status MEDLINE
Authors Hoplight BJ. Vincow ES. Neumaier JF.
Authors Full Name Hoplight, B J. Vincow, E S. Neumaier, J F.
Institution
Departments of Psychiatry and Behavioral Sciences, Harborview Medical Center, University of Washington, Box
359911, 325 Ninth Avenue, Seattle, WA 98104-2499, USA.
Title
Cocaine increases 5-HT1B mRNA in rat nucleus accumbens shell neurons.
Source
Neuropharmacology. 52(2):444-9, 2007 Feb.
Journal Name
Neuropharmacology
Country of Publication
England
Abstract
Serotonin 5-HT(1B) receptors modulate behavioral responses to cocaine, but the effects of
cocaine on endogenous 5-HT(1B) receptor expression are not known. Therefore, we
examined the effect of binge cocaine administration on 5-HT1B mRNA expression in rat brain.
We found that chronic, but not acute, binge cocaine exposure increased 5-HT(1B) mRNA by
approximately 80% in nucleus accumbens shell and dorsal striatum. Surprisingly, 5-HT(1B)
mRNA was increased in nucleus accumbens shell after chronic vehicle treatment as well, but
this effect was driven by animals that were housed with cocaine-treated animals. Thus, 5HT(1B) mRNA is upregulated by repeated exposure to cocaine and perhaps by social stress
as well; both of these factors are relevant to the risk for relapse in cocaine addiction.
ISSN Print 0028-3908
Publication Type Journal Article. Research Support, N.I.H., Extramural.
Date of Publication 2007 Feb
Year of Publication 2007
Issue/Part 2
Volume 52
Page 444-9
COCAINE 2007 <813>
Database EMBASE
Accession Number 2006626689
Authors McKenzie K.M. Mee J.M. Rogers C.J. Hixon M.S. Kaufmann G.F. Janda K.D.
Institution
(McKenzie, Mee, Rogers, Hixon, Kaufmann, Janda) The Skaggs Institute for Chemical Biology, Departments of
Chemistry and Immunology, The Worm Institute of Research and Medicine, La Jolla, CA 92037, United States.
Country of Publication
United Kingdom
Title
Identification and Characterization of Single Chain Anti-cocaine Catalytic Antibodies.
Source
Journal of Molecular Biology. 365(3)(pp 722-731), 2007. Date of Publication: 19 Jan 2007.
Abstract
Cocaine is a powerful and addictive stimulant whose abuse remains a prevalent health and
societal crisis. Unfortunately, no pharmacological therapies exist and therefore alternative
protein-based
therapies
have
been
examined.
One
such
approach
is
immunopharmacotherapy, wherein antibodies are utilized to either bind or hydrolyze cocaine
thereby blocking it from exerting its euphoric effect. Towards this end, antibodies capable of
binding and hydrolyzing cocaine were identified by phage display from a biased single chain
antibody library generated from the spleens of mice previously immunized with a cocaine
phosphonate transition state analog hapten. Two classes of antibodies emerged based on
sequence homology and mode of action. Alanine scanning mutagenesis and kinetic analysis
revealed that residues H97, H99, and L96 are crucial for antibodies 3F5 and 3H9 to
accelerate the hydrolysis of cocaine. Antibodies 3F1 through 3F4, which are similar to our
previously identified 3A6 class of antibodies, catalyze hydrolysis through transition state
stabilization by tyrosine or histidine residues H50 and L94. Mutation of either one or both
tyrosine residues to histidine conferred hydrolytic activity on previously inactive antibody 3F4.
Mutational analysis of residue H50 of antibody 3F3 resulted in a glutamine mutant with a rate
enhancement three times greater than wild-type. A double mutant, containing glutamineH50
and lysineH52, showed a tenfold rate enhancement over wild-type. These results indicate the
power of initial selection of catalytic antibodies from a biased antibody library in both rapid
generation and screening of mutants for improved catalysis. copyright 2006 Elsevier Ltd. All
rights reserved.
ISSN 0022-2836
Publication Type Journal: Article
Journal Name Journal of Molecular Biology
Volume 365
Issue Part 3
Page 722-731
Year of Publication 2007
Date of Publication 19 Jan 2007
COCAINE 2007 <818>
Database EMBASE
Accession Number 2006614860
Authors Salloum I.M. Douaihy A. Cornelius J.R. Kirisci L. Kelly T.M. Hayes J.
Institution
(Salloum, Douaihy, Cornelius, Kelly, Hayes) Western Psychiatric Institute, Clinic, the University of Pittsburgh
Medical Center, 3811 O'Hara Street, Pittsburgh, PA 15213, United States.
(Kirisci) Pharmaceutical Sciences, School of Pharmacy, University of Pittsburgh, Pittsburgh, PA 15213, United
States.
Country of Publication
United Kingdom
Title
Divalproex utility in bipolar disorder with co-occurring cocaine dependence: A pilot
study.
Source
Addictive Behaviors. 32(2)(pp 410-415), 2007. Date of Publication: Feb 2007.
Abstract
Objective: The aim of this open-label pilot study was to evaluate the utility of divalproex in
decreasing cocaine use and stabilizing mood symptoms among patients with bipolar disorder
with comorbid cocaine dependence. Method: Fifteen patients enrolled in the study and seven
met final inclusion criteria of DSM-IV/SCID diagnoses of bipolar I disorder and comorbid
cocaine dependence with active cocaine use. Patients were started on open-label divalproex.
After stabilization on divalproex sodium, weekly assessments were undertaken for 8 weeks.
Subjects also attended dual recovery counseling. Results: The results revealed significant
improvement on % cocaine abstinent days, dollars spent on cocaine, ASI's drug use severity
index, % alcohol abstinent days, drinks per drinking day, marijuana use and cigarettes
smoking. They also had significant improvement on manic, depressive, and sleep symptoms
and on functioning. There were no reported adverse events or increases in liver function
tests. Conclusion: The results of this open-label study point to the potential utility of divalproex
in patients with bipolar disorder and primary cocaine dependence. Double-blind, placebocontrolled studies to fully evaluate the efficacy of divalproex in this high risk clinical population
are warranted. copyright 2006 Elsevier Ltd. All rights reserved.
ISSN 0306-4603
Publication Type Journal: Article
Journal Name Addictive Behaviors
Volume 32
Issue Part 2
Page 410-415
Year of Publication 2007
Date of Publication Feb 2007
COCAINE 2007 <825>
Database EMBASE
Accession Number 2006604932
Authors Gilbert K.M. Boos T.L. Dersch C.M. Greiner E. Jacobson A.E. Lewis D. Matecka D. Prisinzano T.E. Zhang
Y. Rothman R.B. Rice K.C. Venanzi C.A.
Institution
(Gilbert, Venanzi) Department of Chemistry and Environmental Science, New Jersey Institute of Technology,
University Heights, Newark, NJ 07102, United States.
(Boos, Greiner, Jacobson, Lewis, Matecka, Prisinzano, Zhang, Rice) Laboratory of Medicinal Chemistry, National
Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, United
States.
(Dersch, Rothman) Clinical Psychopharmacology Section, Intramural Research Program, National Institute on Drug
Abuse, Baltimore, MD 21224, United States.
Country of Publication
United Kingdom
Title
DAT/SERT selectivity of flexible GBR 12909 analogs modeled using 3D-QSAR
methods.
Source
Bioorganic and Medicinal Chemistry. 15(2)(pp 1146-1159), 2007. Date of Publication: 15
Jan 2007.
Abstract
The dopamine reuptake inhibitor GBR 12909 (1-{2-[bis(4-fluorophenyl)methoxy]ethyl}-4-(3phenylpropyl)piperazine, 1) and its analogs have been developed as tools to test the
hypothesis that selective dopamine transporter (DAT) inhibitors will be useful therapeutics for
cocaine addiction. This 3D-QSAR study focuses on the effect of substitutions in the
phenylpropyl region of 1. CoMFA and CoMSIA techniques were used to determine a
predictive and stable model for the DAT/serotonin transporter (SERT) selectivity (represented
by pK_i (DAT/SERT)) of a set of flexible analogs of 1, most of which have eight
rotatable bonds. In the absence of a rigid analog to use as a 3D-QSAR template, six
conformational families of analogs were constructed from six pairs of piperazine and
piperidine template conformers identified by hierarchical clustering as representative
molecular conformations. Three models stable to y-value scrambling were identified after a
comprehensive CoMFA and CoMSIA survey with Region Focusing. Test set correlation
validation led to an acceptable model, with q² = 0.508, standard error of
prediction = 0.601, two components, r² = 0.685, standard error of estimate =
0.481, F value = 39, percent steric contribution = 65, and percent electrostatic contribution =
35. A CoMFA contour map identified areas of the molecule that affect pK_i
(DAT/SERT). This work outlines a protocol for deriving a stable and predictive model of the
biological activity of a set of very flexible molecules. copyright 2006 Elsevier Ltd. All rights
reserved.
ISSN 0968-0896
Publication Type Journal: Article
Journal Name Bioorganic and Medicinal Chemistry
Volume 15
Issue Part 2
Page 1146-1159
Year of Publication 2007
Date of Publication 15 Jan 2007
COCAINE 2007 <828>
Database EMBASE
Accession Number 2006600370
Authors Poon H.F. Abdullah L. Mullan M.A. Mullan M.J. Crawford F.C.
Institution
(Poon, Abdullah, Mullan, Mullan, Crawford) Roskamp Institute, 2040 Whitfield Ave, Sarasota, FL 34243, United
States.
Country of Publication
United Kingdom
Title
Cocaine-induced oxidative stress precedes cell death in human neuronal progenitor
cells.
Source
Neurochemistry International. 50(1)(pp 69-73), 2007. Date of Publication: Jan 2007.
Abstract
By 2003, an estimated 34 million Americans had used cocaine according to the National
Survey on Drug Use & Health. About 5.9 million of those had used in the past 12 months.
Chronic cocaine users often develop addiction, dependency and tolerance to the drug. The
psychological and physical effects of cocaine are due to the disruption of the limbic system in
the central nervous system (CNS). Increased oxidative stress reported in the frontal cortex
and the striatum of rats exposed to cocaine suggests that oxidative damage plays a
significant role in cocaine-induced disruption of the CNS. Although it is evident that cocaine
induces oxidative stress in the CNS, little has been learned about whether such increased
oxidative stress is also relevant to apoptosis in cocaine-exposed models. To gain insight into
the role of cocaine-induced oxidative stress in apoptosis, we hypothesized that oxidative
stress precedes cell death when cocaine is administrated. To test this hypothesis, we have
monitored the oxidative stress and apoptotic effects of acute cocaine exposure in human
neuronal progenitor cells (HNPC). We found that oxidative stress was significantly increased
at 48 h after a 30 min cocaine exposure compared to control cells, and that this was followed
by cell death at 72 h. Using the same experimental paradigm we have previously shown that
pro-inflammatory genes are up-regulated in cocaine-exposed HNPC at 24 h. Therefore, we
suggest that the increased oxidative stress (possibly mediated by inflammatory responses)
precedes cell death in cocaine-exposed HNPC. This may have implications for the
consequences of cocaine abuse in situations where antioxidant capacity is compromised, as
in the aging brain. copyright 2006 Elsevier Ltd. All rights reserved.
ISSN 0197-0186
Publication Type Journal: Article
Journal Name Neurochemistry International
Volume 50
Issue Part 1
Page 69-73
Year of Publication 2007
Date of Publication Jan 2007
COCAINE 2007 <836>
Database EMBASE
Accession Number 2007614354
Authors Peoples L.L. Kravitz A.V. Guillem K.
Institution
(Peoples, Kravitz, Guillem) Department of Psychiatry, University of Pennsylvania School of Medicine, Philadelphia,
PA 19104, United States.
(Peoples, Kravitz) Neuroscience Graduate Group, University of Pennsylvania School of Medicine, Philadelphia, PA
19104, United States.
Country of Publication
United Kingdom
Title
The role of accumbal hypoactivity in cocaine addiction.
Source
TheScientificWorldJournal. 7(SUPPL. 2)(pp 22-45), 2007. Date of Publication: 02 Nov 2007.
Abstract
Cocaine-induced hypoactivity of the nucleus accumbens (NAC) is hypothesized to contribute
to cocaine addiction. There are two important questions related to this hypothesis. First,
cocaine addiction is characterized by an increase in drug-directed behavior and a
simultaneous weakening of other motivated behaviors. However, the NAC contributes to both
drug- and nondrug-directed behavior. Moreover, the nature of the contributions is similar and
associated predominantly with excitatory phasic firing patterns. Given these observations, it is
not clear how hypoactivity of NAC neurons might contribute to the behaviors that characterize
cocaine addiction. Second, various types of investigations have documented neurochemical
and molecular adaptations that could underlie NAC hypoactivity. However, there is also
evidence of other adaptations in the NAC and in NAC afferents, which are expected to have
an excitatory influence on NAC neural activity. In the present review, we will briefly overview
these issues. We will also describe a hypothesis and related empirical evidence that may
contribute to answering these questions. Further investigation of the issues and the
hypothesis may contribute to a better understanding of the neuroadaptations that contribute to
cocaine addiction. copyright2007 with author. Published by TheScientificWorld.
ISSN 1537-744X
Publication Type Journal: Short Survey
Journal Name TheScientificWorldJournal
Volume 7
Issue Part SUPPL. 2
Page 22-45
Year of Publication 2007
Date of Publication 02 Nov 2007
COCAINE 2007 <866>
Database EMBASE
Accession Number 2007561466
Authors Felszeghy K. Espinosa J.M. Scarna H. Berod A. Rostene W. Pelaprat D.
Institution
(Felszeghy, Espinosa, Rostene, Pelaprat) INSERM, U 339, Hopital Saint-Antoine, Paris Cedex, France.
(Scarna, Berod) Laboratoire de Neuropharmacologie, Faculte de Pharmacie, Universite Lyon 1, Lyon Cedex,
France.
(Felszeghy) Brain Physiology Research Group, Hungarian Academy of Sciences, Semmelweiss University,
Budapest, Hungary.
(Espinosa) Laboratoire PIOM, CNRS UMR5501, 33607 Pessac, France.
(Rostene) INSERM, U 732, Hopital Saint-Antoine, 75571 Paris Cedex 12, France.
(Pelaprat) INSERM, U 773, CRB3, Faculte de Medecine Xavier Bichat, 16 rue Henri Huchard, 75870 Paris Cedex
18, France.
Country of Publication
United Kingdom
Title
Neurotensin receptor antagonist administered during cocaine withdrawal decreases
locomotor sensitization and conditioned place preference.
Source
Neuropsychopharmacology. 32(12)(pp 2601-2610), 2007. Date of Publication: Dec 2007.
Abstract
Chronic use of psychostimulants induces enduringly increased responsiveness to a
subsequent psychostimulant injection and sensitivity to drug-associated cues, contributing to
drug craving and relapse. Neurotensin (NT), a neuropeptide functionally linked to
dopaminergic neurons, was suggested to participate in these phenomena. We and others
have reported that SR 48692, an NT receptor antagonist, given in pre- or cotreatments with
cocaine or amphetamine, alters some behavioral effects of these drugs in rats. However, its
efficacy when applied following repeated cocaine administration remains unknown. We,
therefore, evaluated the ability of SR 48692, administered after a cocaine regimen, to
interfere with the expression of locomotor sensitization and conditioned place preference
(CPP) in rats. We demonstrated that the expression of locomotor sensitization, induced by
four cocaine injections (15 mg/kg, i.p.) every other day and a cocaine challenge 1 week later,
was attenuated by a subsequent 2-week daily administration of SR 48692 (1 mg/kg, i.p.).
Furthermore, the expression of cocaine-induced CPP was suppressed by a 10-day SR 48692
treatment started after the conditioning period (four 15 mg/kg cocaine injections every other
day). Taken together, our data show that a chronic SR 48692 treatment given after a cocaine
regimen partly reverses the expression of locomotor sensitization and CPP in the rat,
suggesting that NT participates in the maintenance of these behaviors. Our results support
the hypothesis that targeting neuromodulatory systems, such as the NT systems may offer
new strategies in the treatment of drug addiction. copyright 2007 Nature Publishing Group All
rights reserved.
ISSN 0893-133X
Publication Type Journal: Article
Journal Name Neuropsychopharmacology
Volume 32
Issue Part 12
Page 2601-2610
Year of Publication 2007
Date of Publication Dec 2007
COCAINE 2007 <872>
Database EMBASE
Accession Number 2007529649
Authors Tanda G.
Institution
(Tanda) Psychobiology Section, Medications Discovery Research Branch, National Institute Drug Abuse, National
Institutes Health, Department of Health and Human Services, 5500 Nathan Shock Drive, Baltimore, MD 21224,
United States.
Country of Publication
United Kingdom
Title
Modulation of the endocannabinoid system: Therapeutic potential against cocaine
dependence.
Source
Pharmacological Research. 56(5)(pp 406-417), 2007. Date of Publication: Nov 2007.
Abstract
Dependence on cocaine is still a main unresolved medical and social concern, and in spite
of research efforts, no pharmacological therapy against cocaine dependence is yet available.
Recent studies have shown that the endocannabinoid system participates in specific stages
and aspects of drug dependence in general, and some of this evidence suggests an
involvement of the cannabinoid system in cocaine effects. For example, cocaine
administration has been shown to alter brain endocannabinoid levels, and the
endocannabinoid system has been involved in long-term modifications of brain processes that
might play a role in neuro/behavioral effects of psychostimulant drugs like cocaine. Human
studies show that marijuana dependence is frequently associated with cocaine dependence,
and that the cannabinoid receptor CNR1 gene polymorphism might be related to cocaine
addiction. This article will review the main papers in the field showing how a modulation of
different components of the cannabinoid system might interact with some of the
neurobiological/behavioral effects of cocaine related to its reinforcing effects, evaluated in
preclinical models or in clinical settings. The goal of this review will be to provide insights into
the complex picture of cocaine abuse and addiction, and to extrapolate from such
endocannabinoid-cocaine interactions useful information to test the therapeutic potential of
cannabinoid ligands and endocannabinoid-level enhancers against cocaine dependence for
future preclinical/clinical trials.
ISSN 1043-6618
Publication Type Journal: Review
Journal Name Pharmacological Research
Volume 56
Issue Part 5
Page 406-417
Year of Publication 2007
Date of Publication Nov 2007
COCAINE (A) 2007 <885>
Database EMBASE
Accession Number 2007558043
Authors Boyer F. Dreyer J.-L.
Institution
(Boyer, Dreyer) Institute of Biochemistry, University of Fribourg, Rue du Musee 5, CH-1700 Fribourg, Switzerland.
Country of Publication
United Kingdom
Title
Alpha-synuclein in the nucleus accumbens induces changes in cocaine behaviour in
rats.
Source
European Journal of Neuroscience. 26(10)(pp 2764-2776), 2007. Date of Publication: Nov
2007.
Abstract
The mesolimbic dopaminergic system is widely recognized to be critical to the neurobiology
of cocaine reward and addiction. The neuronal protein, alpha-synuclein, is an important
regulator in dopaminergic transmission. It interacts with the dopamine transporter, and
regulates dopaminergic content, neurotransmission and synaptic strength of dopaminergic
neurons. Alpha-synuclein levels are elevated in midbrain dopamine neurons of chronic
cocaine abusers, and its expression is increased in psychostimulant-treated animals [M.S.
Brenz-Verca et al. (2003) J. Neurosci., 18, 1923-1938]. This suggests a role for alphasynuclein in psychostimulant-induced behavioural effects. To investigate this hypothesis, we
tested the effect of stimulation and silencing of alpha-synuclein expression in the nucleus
accumbens (NAcc) on two cocaine-induced behavioural effects in the rat. For this purpose,
animals were administered with lentiviruses driving alpha-synuclein overexpression under the
control of a doxycycline regulatable promoter and/or with three lentiviruses expressing targetspecific siRNAs, aimed at silencing alpha-synuclein mRNA expression. Animals were then
tested for cocaine-induced locomotion (15 mg/kg i.p.) or cocaine-induced intravenous selfadministration (SA; 0.7 mg/kg, 1 h/day). Overexpression of alpha-synuclein in the NAcc
induced a 45% increase in locomotor activity and a 1.9-fold increase of cocaine SA, which
could be abolished when the same animal was fed doxycycline. Furthermore, local inhibition
of alpha-synuclein in the NAcc resulted in significant hypolocomotion activity and a decrease
in SA. Our results demonstrate that alpha-synuclein is able to modulate cocaine-induced
behavioural effects. This suggests that targeting alpha-synuclein function could provide new
therapeutic strategies to treat cocaine abuse, for which there is no available treatment.
copyright The Authors (2007).
ISSN 0953-816X
Publication Type Journal: Article
Journal Name European Journal of Neuroscience
Volume 26
Issue Part 10
Page 2764-2776
Year of Publication 2007
Date of Publication Nov 2007
COCAINE (A) 2007 <918>
Database EMBASE
Accession Number 2007489851
Authors Xi Z.-X. Yang Z. Li S.-J. Li X. Dillon C. Peng X.-Q. Spiller K. Gardner E.L.
Institution
(Xi, Li, Dillon, Peng, Spiller, Gardner) Intramural Research Program, National Institute on Drug Abuse, National
Institutes of Health, Baltimore, MD 21224, United States.
(Yang) Beijing Institute of Basic Medical Sciences, Beijing, China.
(Li) Department of Biophysics, Medical College of Wisconsin, Milwaukee, WI 53226, United States.
Country of Publication
United Kingdom
Title
Levo-tetrahydropalmatine inhibits cocaine's rewarding effects: Experiments with selfadministration and brain-stimulation reward in rats.
Source
Neuropharmacology. 53(6)(pp 771-782), 2007. Date of Publication: Nov 2007.
Abstract
It was recently reported that levo-tetrahydropalmatine (l-THP), a dopamine (DA)
D₁ and D₂ receptor antagonist purified from the Chinese herb
Stephanie, appears to be effective in attenuating cocaine self-administration, cocainetriggered reinstatement and cocaine-induced conditioned place preference in preclinical
animal models. The present study was designed to contrast l-THP's effects on cocaine selfadministration under fixed-ratio (FR) and progressive-ratio (PR) reinforcement, and to study lTHP's effects on cocaine-enhanced brain stimulation reward (BSR). Systemic administration
of l-THP produced dose-dependent, biphasic effects, i.e., low-to-moderate doses (1, 3, 10
mg/kg) increased, while a high dose (20 mg/kg) inhibited cocaine self-administration behavior
under FR2 reinforcement. The increased cocaine self-administration is likely a compensatory
response to a reduction in cocaine's rewarding effects, because the same low doses of l-THP
dose-dependently attenuated cocaine self-administration under PR reinforcement and also
attenuated cocaine-enhanced BSR. These attenuations of PR cocaine self-administration and
cocaine-enhanced BSR are unlikely due to l-THP-induced sedation or locomotor inhibition,
because only 10 mg/kg, but not 1-3 mg/kg, of l-THP inhibited locomotion, sucrose selfadministration and asymptotic operant performance in the BSR paradigm. In vivo
microdialysis demonstrated that l-THP slightly elevates extracellular nucleus accumbens DA
by itself, but dose-dependently potentiates cocaine-augmented DA, suggesting that a
postsynaptic, rather than presynaptic, DA receptor antagonism underlies l-THP's actions on
cocaine reward. Together, the present data, combined with previous findings, support the
potential use of l-THP for treatment of cocaine addiction. copyright 2007 Elsevier Ltd. All
rights reserved.
ISSN 0028-3908
Publication Type Journal: Article
Journal Name Neuropharmacology
Volume 53
Issue Part 6
Page 771-782
Year of Publication 2007
Date of Publication Nov 2007
COCAINE (A) 2007 <997>
Database EMBASE
Accession Number 2007423660
Authors Bailey A. Yoo J.H. Racz I. Zimmer A. Kitchen I.
Institution
(Bailey, Yoo, Kitchen) School of Biomedical and Molecular Sciences, University of Surrey, Guildford, United
Kingdom.
(Racz, Zimmer) Department of Molecular Psychiatry, Life and Brain Center, University of Bonn, Bonn, Germany.
(Bailey) School of Biomedical and Molecular Sciences, University of Surrey, Guildford, Surrey, GU2 7XH, United
Kingdom.
Country of Publication
United Kingdom
Title
Preprodynorphin mediates locomotion and D₂ dopamine and mu-opioid
receptor changes induced by chronic 'binge' cocaine administration.
Source
Journal of Neurochemistry. 102(6)(pp 1817-1830), 2007. Date of Publication: Sep 2007.
Abstract
Evidence suggests that the kappa-opioid receptor (KOP-r) system plays an important role in
cocaine addiction. Indeed, cocaine induces endogenous KOP activity, which is a mechanism
that opposes alterations in behaviour and brain function resulting from repeated cocaine use.
In this study, we have examined the influence of deletion of preprodynorphin (ppDYN) on
cocaine-induced behavioural effects and on hypothalamic-pituitary-adrenal axis activity.
Furthermore, we have measured mu-opioid receptor (MOP-r) agonist-stimulated
[³⁵S]GTPgammaS, dopamine D₁, D₂ receptor and
dopamine transporter (DAT) binding. Male wild-type (WT) and ppDYN knockout (KO) mice
were injected with saline or cocaine (45 mg/kg/day) in a 'binge' administration paradigm for 14
days. Chronic cocaine produced an enhancement of locomotor sensitisation in KO. No
genotype effect was found on stereotypy behaviour. Cocaine-enhanced MOP-r activation in
WT but not in KO. There was an overall decrease in D₂ receptor binding in
cocaine-treated KO but not in WT mice. No changes were observed in D₁ and
DAT binding. Cocaine increased plasma corticosterone levels in WT but not in KO. The data
confirms that the endogenous KOP system inhibits dopamine neurotransmission and that
ppDYN may mediate the enhancement of MOP-r activity and the activation of the
hypothalamic-pituitary-adrenal axis after chronic cocaine treatment. copyright 2007 The
Authors.
ISSN 0022-3042
Publication Type Journal: Article
Journal Name Journal of Neurochemistry
Volume 102
Issue Part 6
Page 1817-1830
Year of Publication 2007
Date of Publication Sep 2007
COCAINE 2007 <149>
Database EMBASE
Accession Number 2007080125
Authors Muller C.P. De Souza Silva M.A. Huston J.P.
Institution
(Muller, De Souza Silva, Huston) Institute of Physiological Psychology I, Centre for Biological and Medical
Research, University of Dusseldorf, Universitatsstrasse 1, 40225 Dusseldorf, Germany.
Country of Publication
United Kingdom
Title
Double dissociating effects of sensory stimulation and cocaine on serotonin activity
in the occipital and temporal cortices.
Source
Neuropharmacology. 52(3)(pp 854-862), 2007. Date of Publication: Mar 2007.
Abstract
Visual cues that become associated with the consumption of psychostimulant drugs
energize craving and the intake of the drug by mechanisms of which little is known. In two
experiments using in vivo microdialysis in freely moving rats we compared the effects of
visual and auditory stimulation with that of cocaine (0, 5, 10, 20 mg/kg; i.p.) on the
extracellular serotonin (5-HT) activity in the occipital and temporal cortices in relation to
behavior. Visual stimulation increased 5-HT in the occipital, but not temporal cortex, parallel
to an increase in locomotion. Auditory stimulation decreased 5-HT in the auditory, but not
occipital cortex, thus, showing a double dissociated 5-HT response. These data suggest that
a locally restricted 5-HT response to sensory stimulation may gate behavioral activity sensemodality selectively. Cocaine affected 5-HT in the occipital cortex and behavioral activity in
the same direction as visual stimulation, but in an amplified and prolonged way. In the
temporal cortex cocaine also caused an increase in 5-HT. The findings demonstrate common
effects of visual stimulation and cocaine on 5-HT activity in the occipital cortex in relation to
locomotor activity. The results suggest that concepts of how neutral visual cues become
powerful energizers of addiction-related behaviors should be expanded to incorporate not
only an acute enhancement of reward processing mechanisms, but, in parallel, also an
amplified processing of visual stimuli in the occipital cortex. copyright 2006 Elsevier Ltd. All
rights reserved.
ISSN 0028-3908
Publication Type Journal: Article
Journal Name Neuropharmacology
Volume 52
Issue Part 3
Page 854-862
Year of Publication 2007
Date of Publication Mar 2007
COCAINE 2007 <165>
Database EMBASE
Accession Number 2007042788
Authors Goldstein R.Z. Tomasi D. Rajaram S. Cottone L.A. Zhang L. Maloney T. Telang F. Alia-Klein N. Volkow N.D.
Institution
(Goldstein, Tomasi, Cottone, Maloney, Telang, Alia-Klein) Brookhaven National Laboratory, P.O. Box 5000, Upton,
NY 11973-5000, United States.
(Rajaram, Zhang) State University of New York at Stony Brook, Stony Brook, NY 11794-4400, United States.
(Volkow) National Institute on Drug Abuse, Bethesda, MD 20892, United States.
Country of Publication
United Kingdom
Title
Role of the anterior cingulate and medial orbitofrontal cortex in processing drug cues
in cocaine addiction.
Source
Neuroscience. 144(4)(pp 1153-1159), 2007. Date of Publication: 23 Feb 2007.
Abstract
Our goal in the current report was to design a new functional magnetic resonance imaging
(fMRI) task to probe the role of the anterior cingulate cortex (ACC) and orbitofrontal cortex
(OFC) in processing of salient symptom-related cues during the simultaneous performance of
an unrelated task in drug-addicted persons. We used a novel fMRI color-word drug Stroop
task in 14 individuals with cocaine use disorders; subjects had to press for color of drug vs.
matched neutral words. Although there were no accuracy or speed differences between the
drug and neutral conditions in the current sample of subjects, drug words were more
negatively valenced than the matched neutral words. Further, consistent with prior reports in
individuals with other psychopathologies using different Stroop fMRI paradigms, our more
classical color-word Stroop design revealed bilateral activations in the caudal-dorsal anterior
cingulate cortex (cdACC) and hypoactivations in the rostro-ventral anterior cingulate
cortex/medial orbitofrontal cortex (rACC/mOFC). A trend for larger rACC/mOFC
hypoactivations to the drug than neutral words did not survive whole-brain corrections.
Nevertheless, correlation analyses indicated that (1) the more the cdACC drug-related
activation, the more negative the valence attributed to the drug words (r=-0.86, P<0.0001) but
not neutral words; and (2) the more the rACC/mOFC hypoactivation to drug minus neutral
words, the more the errors committed specifically to the drug minus neutral words (r=0.85,
P<0.0001). Taken together, results suggest that this newly developed drug Stroop fMRI task
may be a sensitive biobehavioral assay of the functions recruited for the regulation of
responses to salient symptom-related stimuli in drug-addicted individuals. copyright 2006
IBRO.
ISSN 0306-4522
Publication Type Journal: Article
Journal Name Neuroscience
Volume 144
Issue Part 4
Page 1153-1159
Year of Publication 2007
Date of Publication 23 Feb 2007
COCAINE (A) 2007 <167>
Database EMBASE
Accession Number 2007042551
Authors Hoplight B.J. Vincow E.S. Neumaier J.F.
Institution
(Hoplight, Vincow, Neumaier) Departments of Psychiatry and Behavioral Sciences, Harborview Medical Center,
University of Washington, 325 Ninth Avenue, Seattle, WA 98104-2499, United States.
Country of Publication
United Kingdom
Title
Cocaine increases 5-HT_1B mRNA in rat nucleus accumbens shell
neurons.
Source
Neuropharmacology. 52(2)(pp 444-449), 2007. Date of Publication: Feb 2007.
Abstract
Serotonin 5-HT_1B receptors modulate behavioral responses to cocaine, but the
effects of cocaine on endogenous 5-HT_1B receptor expression are not known.
Therefore, we examined the effect of binge cocaine administration on 5-HT1B mRNA
expression in rat brain. We found that chronic, but not acute, binge cocaine exposure
increased 5-HT_1B mRNA by [similar to]80% in nucleus accumbens shell and
dorsal striatum. Surprisingly, 5-HT_1B mRNA was increased in nucleus
accumbens shell after chronic vehicle treatment as well, but this effect was driven by animals
that were housed with cocaine-treated animals. Thus, 5-HT_1B mRNA is
upregulated by repeated exposure to cocaine and perhaps by social stress as well; both of
these factors are relevant to the risk for relapse in cocaine addiction. copyright 2006 Elsevier
Ltd. All rights reserved.
ISSN 0028-3908
Publication Type Journal: Article
Journal Name Neuropharmacology
Volume 52
Issue Part 2
Page 444-449
Year of Publication 2007
Date of Publication Feb 2007
COCAINE (A) 2007 <172>
Database EMBASE
Accession Number 2007037085
Authors Mantsch J.R. Katz E.S.
Institution
(Mantsch, Katz) Department of Biomedical Sciences, Marquette University, Milwaukee, WI, United States.
(Mantsch) Department of Biomedical Sciences, Marquette University, Schroeder Health Complex, PO Box 1881,
Milwaukee, WI 53201-1881, United States.
Country of Publication
United Kingdom
Title
Elevation of glucocorticoids is necessary but not sufficient for the escalation of
cocaine self-administration by chronic electric footshock stress in rats.
Source
Neuropsychopharmacology. 32(2)(pp 367-376), 2007. Date of Publication: Feb 2007.
Abstract
The examination of cocaine self-administration (SA) by rats under conditions that promote
escalating patterns of intake should lead to a better understanding of factors that contribute to
cocaine addiction. This study investigated the ability of repeated daily exposure to a stressor,
electric footshock (EFS), to escalate cocaine SA. Male Sprague-Dawley rats were trained to
self-administer cocaine (0.5 mg/kg/inf, i.v.) by pressing a lever under a FR4 schedule during
2-h sessions comprised of four 30-min SA components. Repeated daily EFS consisting of
shock sequences (3 x 0.6 mA, 100-ms duration, 1-s frequency) delivered under a variable
time 45-s schedule for 5 min before each of the four SA components across 14 days of SA
testing produced a significant escalation of cocaine SA. EFS failed to escalate food-reinforced
lever pressing and did not alter cocaine SA when administered either inside or outside of the
SA context 4 h after daily SA testing. Surgical adrenalectomy along with diurnal
corticosterone (CORT) replacement prevented EFS-induced escalation without altering SA in
the absence of EFS, indicating that increases in circulating glucocorticoids were necessary for
the escalating effects of EFS. Elevation of CORT through repeated daily CORT injections (3.0
mg/kg, i.p.) failed to reproduce the effects of repeated daily EFS on SA, but restored the
escalating effects of EFS in adrenalectomized rats with CORT replacement, suggesting that
an elevation of glucocorticoids was necessary but alone was not sufficient for the escalation
of cocaine SA by EFS. copyright 2007 Nature Publishing Group. All rights reserved.
ISSN 0893-133X
Publication Type Journal: Article
Journal Name Neuropsychopharmacology
Volume 32
Issue Part 2
Page 367-376
Year of Publication 2007
Date of Publication Feb 2007
COCAINE (A) 2007 <173>
Database EMBASE
Accession Number 2007037084
Authors Edwards S. Whisler K.N. Fuller D.C. Orsulak P.J. Self D.W.
Institution
(Edwards, Whisler, Fuller, Orsulak, Self) Department of Psychiatry, Seay Center for Basic and Applied Research in
Psychiatric Illness, University of Texas Southwestern Medical Center, Dallas, TX, United States.
(Self) Department of Psychiatry, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas,
TX 75390-9070, United States.
Country of Publication
United Kingdom
Title
Addiction-related alterations in D₁ and D₂ dopamine
receptor behavioral responses following chronic cocaine self-administration.
Source
Neuropsychopharmacology. 32(2)(pp 354-366), 2007. Date of Publication: Feb 2007.
Abstract
The cocaine-addicted phenotype can be modeled in rats based on individual differences in
preferred levels of cocaine intake and a propensity for relapse in withdrawal. These cocainetaking and -seeking behaviors are strongly but differentially regulated by postsynaptic
D₁ and D₂ receptors in the mesolimbic dopamine system. Thus,
we determined whether addiction-related differences in cocaine self-administration would be
related to differential sensitivity in functional D₁ and D₂ receptor
responses. Using a population of 40 outbred Sprague-Dawley rats trained to self-administer
cocaine for 3 weeks, we found that animals with higher preferred levels of cocaine intake
exhibited a vertical and rightward shift in the self-administration dose-response function, and
were more resistant to extinction from cocaine self-administration, similar to phenotypic
changes reported in other models of cocaine addiction. After 3 weeks of withdrawal from
cocaine self-administration, high intake rats were subsensitive to the ability of the
D₁ agonist SKF 81297 to inhibit cocaine-seeking behavior elicited by cocaine
priming, but supersensitive to cocaine seeking triggered by the D₂ agonist
quinpirole, when compared to low intake rats. Additionally, high intake rats developed
profound increases in locomotor responses to D₂ receptor challenge from early
to late withdrawal times, whereas low intake rats developed increased responsiveness to D
₁ receptor challenge. In a second experiment, responses to the mixed
D₁/D₂ agonist apomorphine and the NMDA glutamate receptor
antagonist MK-801 failed to differ between low and high intake rats. These findings suggest
that cocaine addiction is related specifically to differential alterations in functional
D₁ and D₂ receptors and their ability to modulate cocaine-seeking
behavior. copyright 2007 Nature Publishing Group. All rights reserved.
ISSN 0893-133X
Publication Type Journal: Article
Journal Name Neuropsychopharmacology
Volume 32
Issue Part 2
Page 354-366
Year of Publication 2007
Date of Publication Feb 2007
CANNABIS / COCAINE 2007 <233>
Database EMBASE
Accession Number 2007199918
Authors McRae A.L. Hedden S.L. Malcolm R.J. Carter R.E. Brady K.T.
Institution
(McRae, Malcolm, Brady) Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina,
67 President Street, Charleston, SC 29425, United States.
(Hedden, Carter) Department of Biostatistics, Bioinformatics, and Epidemiology, Medical University of South
Carolina, 135 Cannon Street, Charleston, SC 29425, United States.
Country of Publication
United Kingdom
Title
Characteristics of cocaine- and marijuana-dependent subjects presenting for
medication treatment trials.
Source
Addictive Behaviors. 32(7)(pp 1433-1440), 2007. Date of Publication: Jul 2007.
Abstract
Evaluation of the characteristics of individuals presenting for substance abuse treatment can
provide important information to help focus treatment services. In this study, demographic and
clinical characteristics of individuals presenting for medication trials for the treatment of
cocaine or marijuana dependence were compared. Marijuana-dependent subjects were
generally younger than cocaine-dependent subjects, more likely to be Caucasian, and
completed more years of education. Marijuana-dependent subjects also reported significantly
more days using than cocaine-dependent subjects, as well as higher levels of craving. Some
differences in psychiatric symptomatology were also noted, with cocaine-dependent subjects
more likely to report anxiety symptoms and marijuana-dependent subjects reporting more
past depressive episodes. Past and current other drug use was similar between the two
groups. These results highlight the significant impairments associated with marijuana and
cocaine dependence. copyright 2006 Elsevier Ltd. All rights reserved.
ISSN 0306-4603
Publication Type Journal: Article
Journal Name Addictive Behaviors
Volume 32
Issue Part 7
Page 1433-1440
Year of Publication 2007
Date of Publication Jul 2007