Download cocaine 68, 111, 145, 150, 164, 192, 201, 208, 209, 226, 270, 274

COCAINE (A) <2>
Database EMBASE
Accession Number 2006032261
Authors Sun W. Akins C.K. Mattingly A.E. Rebec G.V.
Institution
(Sun, Mattingly, Rebec) Program in Neural Science, Department of Psychology, Indiana University, Bloomington,
IN, United States.
(Akins) Department of Psychology, University of Kentucky, Lexington, KY, United States.
(Rebec) Program in Neural Science, Department of Psychology, Indiana University, 1101 E 10th Street,
Bloomington, IN 47405, United States.
Country of Publication
United Kingdom
Title
Ionotropic glutamate receptors in the ventral tegmental area regulate cocaine-seeking
behavior in rats.
Source
Neuropsychopharmacology. 30(11)(pp 2073-2081), 2005. Date of Publication: Nov 2005.
Abstract
Drug addiction is characterized by compulsive drug-seeking and drug-taking behavior and
by a high rate of relapse even after long periods of abstinence. Although the
mesocorticolimbic dopamine (DA) pathway is thought to play a critical role in drug craving and
relapse, recent evidence also implicates glutamate, an amino acid known to activate DA
neurons in the ventral tegmental area (VTA) via ionotropic receptors. To assess whether
increased glutamate transmission in the VTA is involved in cocaine-primed drug-seeking
behavior, we tested rats in a between-session reinstatement model. They were trained to
press a lever for cocaine infusions (0.25 mg/ infusion) accompanied by compound stimuli
(light and tone) under a modified fixed-ratio 5 reinforcement schedule. Cocaine-primed
reinstatement was conducted after lever pressing was extinguished in the absence of the
conditioned stimuli. Blockade of ionotropic glutamate receptors in the VTA by local application
of kynurenate (0.0, 1.0, 3.2, and 5.6 mug/side) dose-dependently decreased cocaine-primed
reinstatement, whereas sucrose-primed reinstatement of sucrose-seeking behavior was
unaffected. In addition, the minimum effective dose for decreasing cocaine-primed
reinstatement was ineffective in the substantia nigra. Together, these data indicate that
glutamatergic activation of the VTA is critical for cocaine-primed reinstatement. Because such
activation can increase impulse flow in DA neurons and thus DA release in mesocorticolimbic
targets, this glutamate-DA interaction in the VTA may underlie cocaine-primed relapse to
cocaine-seeking behavior. copyright 2005 Nature Publishing Group. All rights reserved.
ISSN 0893-133X
Publication Type Journal: Article
Journal Name Neuropsychopharmacology
Volume 30
Issue Part 11
Page 2073-2081
Year of Publication 2005
Date of Publication Nov 2005
COCAINE (A) <3>
Database EMBASE
Accession Number 2006032260
Authors Slattery D.A. Markou A. Froestl W. Cryan J.F.
Institution
(Slattery, Froestl, Cryan) Psychiatry Program, Novartis Institutes for BioMedical Research, Novartis Pharma AG,
Basel, Switzerland.
(Markou) Department of Neuropharmacology, Scripps Research Institute, San Diego, CA, United States.
(Cryan) Psychiatry Program, Novartis Institutes for BioMedical Research, Novartis Pharma AG, Basel CH-4002,
Switzerland.
Country of Publication
United Kingdom
Title
The GABA<sub>B</sub> receptor-positive modulator GS39783 and the GABA
<sub>B</sub> receptor agonist baclofen attenuate the reward-facilitating effects of
cocaine: Intracranial self-stimulation studies in the rat.
Source
Neuropsychopharmacology. 30(11)(pp 2065-2072), 2005. Date of Publication: Nov 2005.
Abstract
There is an increasing interest in the development of nondopaminergic pharmacotherapies
for cocaine abuse. Emerging preclinical and clinical data with the metabotropic
GABA<sub>B</sub> receptor agonist baclofen support a role for the modulation of
GABA<sub>B</sub> receptors in the treatment of drug addiction. Nevertheless, the muscle
relaxant, hypothermic, and sedative properties of baclofen somewhat limit its widespread
potential therapeutic utility. Recently, positive modulators of the GABA<sub>B</sub> receptor
such as GS39783 (N,N'-dicyclopentyl-2-methylsulfanyl-5-nitro-pyrimidine-4,6-diamine) have
been identified. These positive modulators enhance the effects of GABA (gammaaminobutyric acid) through actions at an allosteric site and are devoid of intrinsic agonistic
efficacy. The aim of the present study was to assess the ability of the novel
GABA<sub>B</sub>-positive modulator GS39873 or baclofen to modulate the behavioral
effects of cocaine. Drugs of abuse such as cocaine lower brain reward thresholds obtained
using intracranial self-stimulation (ICSS). We demonstrate here that GS39783 had no intrinsic
effects on ICSS reward thresholds (10-100 mg/kg p.o.) in rats, whereas the full
GABA<sub>B</sub> receptor agonist baclofen (2.5-5 mg/kg p.o.) dose dependently elevated
thresholds. Moreover, both GS39783 and baclofen attenuated the threshold lowering effect of
cocaine administration (10mg/kg intraperitoneally) in a dose-related manner. These data
strongly suggest that activation of GABA <sub>B</sub> receptors attenuates the rewarding
effects of acute cocaine. Therefore, GABA<sub>B</sub>-positive modulation may represent
a novel therapeutic strategy for the treatment of cocaine dependence and possibly other
drugs of abuse without the side effects of full GABA<sub>B</sub> receptor agonists.
copyright 2005 Nature Publishing Group. All rights reserved.
ISSN 0893-133X
Publication Type Journal: Article
Journal Name Neuropsychopharmacology
Volume 30
Issue Part 11
Page 2065-2072
Year of Publication 2005
Date of Publication Nov 2005
COCAINE <6>
Database EMBASE
Accession Number 2006029819
Authors Soria G. Mendizabal V. Tourino C. Robledo P. Ledent C. Parmentier M. Maldonado R. Valverde O.
Institution
(Soria, Mendizabal, Tourino, Robledo, Maldonado, Valverde) Laboratori de Neurofarmacologia, Departament de
Ciencies Experimentals I de la Salut, Universitat Pompeu Fabra, Barcelona, Spain.
(Robledo) IMIM, Institut Municipal d'Investigadons Mediques, Barcelona, Spain.
(Ledent, Parmentier) IRIBHM, Universite Libre de Bruxelles, Bruxelles, Belgium.
(Valverde) Laboratori de Neurofarmacologia, Universitat Pompeu Fabra, Dr Aiguader 80, Barcelona 08003, Spain.
Country of Publication
United Kingdom
Title
Lack of CBI cannabinoid receptor impairs cocaine self-administration.
Source
Neuropsychopharmacology. 30(9)(pp 1670-1680), 2005. Date of Publication: Sep 2005.
Abstract
Acute rewarding properties are essential for the establishment of cocaine addiction, and
multiple neurochemical processes participate in this complex behavior. In the present study,
we used the self-administration paradigm to evaluate the role of CB1 cannabinoid receptors in
several aspects of cocaine reward, including acquisition, maintenance, and motivation to seek
the drug. For this purpose, both CB1 receptor knockout mice and wild-type littermates were
trained to intravenously self-administer cocaine under different schedules. Several cocaine
training doses (0.32, 1, and 3.2 mg/kg/infusion) were used in the acquisition studies. Only
25% of CB1 knockout mice vs 75% of their wild-type littermates acquired a reliable operant
responding to self-administer the most effective dose of cocaine (1 mg/kg/ infusion), and the
number of sessions required to attain this behavior was increased in knockout mice. Animals
reaching the acquisition criteria were evaluated for the motivational strength of cocaine as a
reinforcer under a progressive ratio schedule. The maximal effort to obtain a cocaine infusion
was significantly reduced after the genetic ablation of CB1 receptors. A similar result was
obtained after the pharmacological blockade of CB1 receptors with SR141716A in wild-type
mice. Moreover, the cocaine dose-response curve was flattened in the knockout group,
suggesting that the differences observed between genotypes were related to changes in the
reinforcing efficacy of the training dose of cocaine. Self-administration for water and food was
not altered in CB1 knockout mice in any of the reinforcement schedules used, which
emphasizes the selective impairment of drug reinforcement in these knockout mice. Finally,
cocaine effects on mesolimbic dopaminergic transmission were evaluated by in vivo
microdialysis in these mice. Acute cocaine administration induced a similar enhancement in
the extracellular levels of dopamine in the nucleus accumbens of both CB1 knockout and
wild-type mice. This work clearly demonstrates that CB1 receptors play an important role in
the consolidation of cocaine reinforcement, although are not required for its acute effects on
mesolimbic dopaminergic transmission. copyright 2005 Nature Publishing Group. All rights
reserved.
ISSN 0893-133X
Publication Type Journal: Article
Journal Name Neuropsychopharmacology
Volume 30
Issue Part 9
Page 1670-1680
Year of Publication 2005
Date of Publication Sep 2005
COCAINE (A) <18>
Database EMBASE
Accession Number 2005575627
Authors Hemby S.E. Tang W. Muly E.C. Kuhar M.J. Howell L. Mash D.C.
Institution
(Hemby) Department of Physiology and Pharmacology, Wake Forest University School of Medicine, WinstonSalem, NC, United States.
(Tang, Muly, Kuhar, Howell) Yerkes National Primate Research Center, Neuroscience Division, Atlanta, GA, United
States.
(Muly, Howell) Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Miami, FL,
United States.
(Kuhar) Department of Pharmacology, Emory University School of Medicine, Miami, FL, United States.
(Mash) Department of Neurology, University of Miami School of Medicine, Miami, FL, United States.
(Hemby) Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, United
States.
Country of Publication
United Kingdom
Title
Cocaine-induced alterations in nucleus accumbens ionotropic glutamate receptor
subunits in human and non-human primates.
Source
Journal of Neurochemistry. 95(6)(pp 1785-1793), 2005. Date of Publication: Dec 2005.
Abstract
Chronic cocaine and withdrawal induce significant alterations in nucleus accumbens (NAc)
glutamatergic function in humans and rodent models of cocaine addiction. Dysregulation of
glutamatergic function of the prefrontal cortical-NAc pathway has been proposed as a critical
substrate for unmanageable drug seeking. Previously, we demonstrated significant upregulation of NMDA, (+/-)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)
and kainate receptor subunit mRNAs and protein levels in the ventral tegmental area (VTA),
but not the substantia nigra, of cocaine overdose victims (COD). The present study was
undertaken to examine the extent of altered ionotropic glutamate receptor (iGluR) subunit
expression in the NAc and the putamen in cocaine overdose victims. Results revealed
statistically significant increases in the NAc, but not in the putamen, of NMDA receptor
subunit (NR)1 and glutamate receptor subunit (GluR)2/3 wit trends in GluR1 and GluR5 in
COD. These results extend our previous finding and indicate pathway-specific alterations in
iGluRs in COD. In order to determine that changes were related to cocaine intake and not to
other factors in the COD victims, we examined the effects of cocaine intravenous selfadministration in rhesus monkeys for 18 months (unit dose of 0.1 mg/kg/injection and daily
drug intake of 0.5 mg/kg/session). Total drug intake for the group of four monkeys was 37.9
+/- 4.6 mg/kg. Statistically significant elevations were observed for NR1, GluR1, GluR2/3 and
GluR5 (p < 0.05) and a trend towards increased NR1 phosphorylated at serine 896 (p = 0.07)
in the NAc but not putamen of monkeys self-administering cocaine compared with controls.
These results extend previous results by demonstrating an up-regulation of NR1, GluR2/3
and GluR5 in the NAc and suggest these alterations are pathway specific. Furthermore, these
changes may mediate persistent drug intake and craving in the human cocaine abuser.
copyright 2005 The Authors. Journal Compilation copyright 2005 International Society for
Neurochemistry.
ISSN 0022-3042
Publication Type Journal: Article
Journal Name Journal of Neurochemistry
Volume 95
Issue Part 6
Page 1785-1793
Year of Publication 2005
Date of Publication Dec 2005
COCAINE / PREGNANCY <68>
Database EMBASE
Accession Number 2005527462
Authors Singer L.T. Eisengart L.J. Minnes S. Noland J. Jey A. Lane C. Min M.O.
Institution
(Singer, Eisengart, Minnes, Jey, Lane, Min) Department of Pediatrics, Case Western Reserve University, The
Triangle Bldg. 11400 Euclid Ave., Cleveland, OH 44106, United States.
(Noland) Vanderbilt University, Nashville, TN, United States.
Country of Publication
United Kingdom
Title
Prenatal cocaine exposure and infant cognition.
Source
Infant Behavior and Development. 28(4)(pp 431-444), 2005. Date of Publication: Dec 2005.
Abstract
The present study examined the relationship of prenatal cocaine exposure to infant
information processing in the first year of life. In a prospective, longitudinal study of 177
cocaine-exposed and 175 non-exposed infants, the Fagan Test of Infant Intelligence (FTII)
was used to measure attention, visual recognition memory and information processing speed
at 6.5 and 12 months of age. Groups were compared over time using mixed linear model
analyses. Prenatal cocaine exposure predicted poorer visual recognition memory at 12
months, with exposed infants obtaining lower mean scores and a higher percentage of scores
in the risk range. Across exposure groups, information processing speed increased with age,
demonstrating a developmental effect. Tobacco and marijuana exposures were related to
faster looking times, which did not relate to visual recognition memory. Cognitive deficits and
attentional problems noted in prior studies of cocaine-exposed children at later ages may be
detectable in infancy. copyright 2005 Elsevier Inc. All rights reserved.
ISSN 0163-6383
Publication Type Journal: Article
Journal Name Infant Behavior and Development
Volume 28
Issue Part 4
Page 431-444
Year of Publication 2005
Date of Publication Dec 2005
COCAINE <75>
Database EMBASE
Accession Number 2005516823
Authors
Hope V.D. Hickman M. Tilling K.
Institution
(Hope, Hickman) Centre for Research on Drugs and Health Behaviour, Imperial College London, London, United
Kingdom.
(Hope) Communicable Disease Surveillance Centre, Health Protection Agency Centre for Infections, Colindale,
London, United Kingdom.
(Tilling) Department of Social Medicine, University of Bristol, Bristol, United Kingdom.
(Hope) Centre for Research on Drugs and Health Behaviour, Imperial College London, Charing Cross Campus, St.
Dunstans Road, London W6 8RP, United Kingdom.
Country of Publication
United Kingdom
Title
Capturing crack cocaine use: Estimating the prevalence of crack cocaine use in
London using capture-recapture with covariates.
Source
Addiction. 100(11)(pp 1701-1708), 2005. Date of Publication: Nov 2005.
Abstract
Aim: To estimate the prevalence of crack cocaine use in 12 London Boroughs (and London
as a whole). Setting: Twelve London Boroughs, 2000-01. Methods: (1) Covariate capturerecapture techniques applied to three data sources of subjects reporting crack cocaine use:
specialist drug treatment (2905), arrest referral (1188) and accident and emergency and
community survey (531); and (2) ratio-estimation multiplier, using an estimate of number of
injecting drug users and proportion that use crack cocaine. Findings: After matching, 4117
individuals aged 15-44 were identified. The best-fitting model estimated 16 855 unobserved
crack cocaine users, giving an overall estimate of approximately 21000 [95% confidence
interval (CI) 13 000-43 000] and a prevalence of 1.5% (95% CI 1.0-3.2%). Prevalence of
crack cocaine use was 2.4% (95% CI 1.5-5.0%) among men and 0.7% (95% CI 0.5-1.0%)
among women, and similar by age groups 15-29 and 30-44 years. Overall, approximately 11
900 (57%) of the estimated number of crack cocaine users were also opiate users. In London
as a whole there may be 46 000 (1.3%) crack cocaine users aged 15-44 years, with 28 000
(1.9%) in inner London-four times higher than estimates from population surveys. Some
corroboration was provided by the ratio-estimation method, which estimated 23 000 users in
the 12 Boroughs. Conclusions: Capture-recapture can be applied to crack cocaine and obtain
better estimates than population surveys. The size of the crack cocaine-using population in
London is large, although currently the majority are also opiate users. Given that half of
current users are under 30 the problems associated with crack cocaine use are likely to
increase in the future. copyright 2005 Society for the Study of Addiction.
ISSN 0965-2140
Publication Type Journal: Article
Journal Name Addiction
Volume 100
Issue Part 11
Page 1701-1708
Year of Publication 2005
Date of Publication Nov 2005
COCAINE <111>
Database EMBASE
Accession Number 2005462402
Authors Przegalinski E. Filip M. Frankowska M. Zaniewska M. Papla I.
Institution
(Przegalinski, Filip, Frankowska, Zaniewska, Papla) Department of Pharmacology, Institute of Pharmacology, Polish
Academy of Sciences, Smetna 12, 31-343 Krakow, Poland.
Country of Publication
United Kingdom
Title
Effects of CP 154,526, a CRF<sub>1</sub> receptor antagonist, on behavioral
responses to cocaine in rats.
Source
Neuropeptides. 39(5)(pp 525-533), 2005. Date of Publication: Oct 2005.
Abstract
We examined the influence of CP 154,526, a selective antagonist of corticotropin-releasing
factor (CRF)<sub>1</sub> receptors, in the locomotor, sensitizing, discriminative stimulus
and rewarding effects of cocaine, as well as on the cocaine-induced reinstatement of cocaineseeking behavior in male Wistar rats. CP 154,526 in doses of 5, 10 and 20 mg/kg, which did
not affect basal locomotor activity, dose-dependently reduced the hyperactivation evoked by
cocaine. To assess the effects of CP 154,526 on the expression of cocaine sensitization, the
rats were injected with either saline or cocaine (10 mg/kg) for 5 days, and were then
challenged with cocaine (10 mg/kg) after pretreatment with saline or CP 154,526 on day 5 of
withdrawal. The cocaine-induced hyperactivity in sensitized rats was reduced by CP 154,526
(10 and 20 mg/kg). In rats trained to discriminate cocaine (10 mg/kg) from saline,
pretreatment with CP 154,526 (5-20 mg/kg) did not affect the cocaine (1.25-10 mg/kg)induced discriminative stimulus effects. In a self-administration model, the rats were trained to
self-administer cocaine (0.5 mg/kg/infusion) in the FR 5 schedule of reinforcement.
Administration of CP 154,526 (10-20 mg/kg) did not alter the rewarding effects of cocaine,
assessed as the number of active-lever presses and infusions; however, following a 10-day
extinction phase, CP 154,526 (5-20 mg/kg) significantly decreased in a dose-dependent
manner the cocaine (10 mg/kg) priming-induced reinstatement of cocaine-seeking behavior.
The present study implies that CRF<sub>1</sub> receptors control the expression of cocaine
hyperactivation and sensitization as well as the cocaine-induced relapse behavior, but do not
play any role in cocaine discrimination and self-administration. These findings may suggest
that CRF<sub>1</sub> receptor antagonists should be considered as possible medications in
the treatment of cocaine addiction. copyright 2005 Elsevier Ltd. All rights reserved.
ISSN 0143-4179
Publication Type Journal: Article
Journal Name Neuropeptides
Volume 39
Issue Part 5
Page 525-533
Year of Publication 2005
Date of Publication Oct 2005
COCAINE <145>
Database EMBASE
Accession Number 2005447109
Authors Meier B.R. Lundy A. Patkar A.A. Weinstein S.
Institution
(Meier, Lundy, Patkar, Weinstein) Thomas Jefferson University, Department of Psychiatry and Human Behavior,
Division of Substance Abuse Programs, 833 Chestnut Street, Philadelphia, PA 19107, United States.
Country of Publication
United Kingdom
Title
The relationship between nicotine dependence and addiction severity amongst
cocaine abusers.
Source
Journal of Substance Use. 10(5)(pp 303-314), 2005. Date of Publication: Oct 2005.
Abstract
The Addiction Severity Index (ASI) and the Fagerstrom Test of Nicotine Dependence
(FTND) are two widely used instruments in their respective domains, but have rarely been
used simultaneously with a substance abuse population. It is argued that the complex link
between nicotine and substance dependence continues not to be well understood, partially
because the measures of smoking in published research with addiction treatment populations
have not been standardized. We studied ASI and FTND responses of 102 crack-cocaine
patients in order to examine the potential utility of using both instruments to enhance our
understanding of these addictions and their relationship to each other. Total FTND scores
were significantly related to ASI drug severity, psychiatric severity and psychiatric composite
scores. Controlling for gender variance yielded similar results. We conclude that using the
FTND does prove to be more sensitive than a less objective measure of smoking, but the ASI
and FTND appear to be psychometrically distinct, making conjoint use for research limited
with some clinical applicability. copyright 2005 Taylor & Francis.
ISSN 1465-9891
Publication Type Journal: Article
Journal Name Journal of Substance Use
Volume 10
Issue Part 5
Page 303-314
Year of Publication 2005
Date of Publication Oct 2005
COCAINE (A) <150>
Database EMBASE
Accession Number 2005443909
Authors Lynch W.J. Taylor J.R.
Institution
(Lynch, Taylor) Department of Psychiatry, Yale University School of Medicine, CMHC, 34 Park Street, New Haven,
CT 06508, United States.
(Lynch) Department of Psychiatric Medicine, University of Virginia Health Sciences, P.O. Box 800623,
Charlottesville, VA 22908, United States.
Country of Publication
United Kingdom
Title
Persistent changes in motivation to self-administer cocaine following modulation of
cyclic AMP-dependent protein kinase A (PKA) activity in the nucleus accumbens.
Source
European Journal of Neuroscience. 22(5)(pp 1214-1220), 2005. Date of Publication: Sep
2005.
Abstract
Drug-induced neuroadaptations within the nucleus accumbens, including activation of
cAMP-dependent protein kinase A (PKA), may contribute to the synaptic plasticity and
behavioural changes that underlie drug addiction. As a direct test of this hypothesis, we
examined the effects in rats of PKA activation (Sp-cAMPS infusions of 10 and 20 nmol/side)
and inhibition (Rp-cAMPS infusions of 10 and 20 nmol/side) in the nucleus accumbens on
motivation to obtain cocaine as measured by responding under the progressive-ratio
schedule. Bilateral infusions of Sp-cAMPS (20 nmol/side) resulted in an increase in
progressive-ratio responding for cocaine and this effect persisted for several days. In contrast,
Rp-cAMPS (20 nmol/side) produced persistent decreases in progressive-ratio responding for
cocaine beginning on the day of administration and lasting for several days. These data
suggest that alternations in PKA activity within the nucleus accumbens as a consequence of
repeated cocaine exposure may contribute to addiction by producing persistent increases in
motivation to obtain cocaine. copyright Federation of European Neuroscience Societies.
ISSN 0953-816X
Publication Type Journal: Article
Journal Name European Journal of Neuroscience
Volume 22
Issue Part 5
Page 1214-1220
Year of Publication 2005
Date of Publication Sep 2005
COCAINE (A) <164>
Database EMBASE
Accession Number 2005416973
Authors Lepsch L.B. Gonzalo L.A. Magro F.J.B. Delucia R. Scavone C. Planeta C.S.
Institution
(Lepsch, Gonzalo, Magro, Planeta) Laboratory of Neuropsychopharmacology, School of Pharmaceutical Sciences,
UNESP- Sao Paulo State University, Sao Paulo, Brazil.
(Delucia, Scavone) Department of Pharmacology, Institute of Biomedical Sciences, University of Sao Paulo, Sao
Paulo, SP, Brazil.
(Planeta) Laboratory of Neuropsychopharmacology, School of Pharmaceutical Sciences, UNESP-Sao Paulo State
University, Rod. Araraquara-Jau Km 1, 14801-902, Araraquara, SP, Brazil.
Country of Publication
United Kingdom
Title
Exposure to chronic stress increases the locomotor response to cocaine and the
basal levels of corticosterone in adolescent rats.
Source
Addiction Biology. 10(3)(pp 251-256), 2005. Date of Publication: Sep 2005.
Abstract
Repeated exposure to stress results in augmentation in the locomotor response to
psychostimulant drugs. We investigated the locomotor response to a novel environment or
cocaine [10 mg/kg, intraperitoneally (i.p.)] and basal corticosterone levels in male adolescent
rats exposed to chronic restraint or variable stress. Animals in the chronic restraint group
were restrained for I hour daily. The chronic variable stress protocol consisted of exposure to
different stressors twice a day in random order. Chronic restraint and variable stress regimens
began simultaneously on postnatal day (P) 25 and were applied for 10 days. During this
period the control group was left undisturbed except for cleaning the cages. Three days after
the last exposure to stress, cocaine- and novelty-induced locomotion were recorded in an
activity cage. Plasma corticosterone levels were determined in a subset of stress and control
animals. Exposure to both chronic restraint and variable stress increased cocaine-induced
locomotion and basal corticosterone plasma levels, while no change was observed in the
response to a novel environment. Moreover, rats exposed to variable stress displayed the
greatest locomotor response following a challenge dose with cocaine when compared to
control and chronic restraint stress groups. This observation indicates that the stress regimen
is relevant to the degree of stress-induced sensitization to cocaine. copyright Society for the
Study of Addiction to Alcohol and Other Drugs.
ISSN 1355-6215
Publication Type Journal: Article
Journal Name Addiction Biology
Volume 10
Issue Part 3
Page 251-256
Year of Publication 2005
Date of Publication Sep 2005
COCAINE (A) <192>
Database EMBASE
Accession Number 2005399987
Authors Radwanska K. Caboche J. Kaczmarek L.
Institution
(Radwanska, Kaczmarek) Laboratory of Molecular Neurobiology, Nencki Insitute, Pasteura 3, 02 093 Warsaw,
Poland.
(Caboche) Laboratory of Neuronal Signaling and Gene Regulation, Universite Pierre et Marie Curie, Paris, France.
Country of Publication
United Kingdom
Title
Extracellular signal-regulated kinases (ERKs) modulate cocaine-induced gene
expression in the mouse amygdala.
Source
European Journal of Neuroscience. 22(4)(pp 939-948), 2005. Date of Publication: Aug
2005.
Abstract
It is known that acute cocaine administration activates the extracellular signal-regulated
kinase (ERK) pathway in the striatum, and results in transcription and translation of immediate
early genes (IEGs). In the present study we investigated a possible involvement of ERK in the
regulation of IEG expression in the amygdala, another brain structure known to be related to
an addicted state. The patterns of cocaine-induced c-Fos, JunB and Zif268 protein expression
were investigated, using an immunohistochemical approach, within distinct nuclei of the
amygdala, either in the presence or absence of a selective inhibitor of the ERK pathway,
SL327. Although these IEGs were similarly activated in the various nuclei of the amygdala
after acute administration of cocaine, they showed different patterns after chronic injections.
They also showed selective sensitivities to ERK inhibition. In particular, whereas c-Fos and
JunB expressions were augmented following chronic cocaine treatment, as compared with
acute treatment, Zif268 expression was decreased by this chronic treatment. Additionally,
chronic blocking of ERK activation affected cocaine-induced c-Fos and JunB but not Zif268
expression. Thus, the differential involvement of ERK in chronic vs. acute regulation of IEGs
may account for its specific role in addiction-related behavioral alterations, such as
sensitization and tolerance. copyright Federation of European Neuroscience Societies.
ISSN 0953-816X
Publication Type Journal: Article
Journal Name European Journal of Neuroscience
Volume 22
Issue Part 4
Page 939-948
Year of Publication 2005
Date of Publication Aug 2005
COCAINE / CANNABIS <201>
Database EMBASE
Accession Number 2005383259
Authors Grant J.D. Scherrer J.F. Lyons M.J. Tsuang M. True W.R. Bucholz K.K.
Institution
(Grant, Scherrer, Bucholz) Department of Psychiatry, Midwest Alcoholism Research Center, Washington University
School of Medicine, 40 N. Kingshighway, St. Louis, MO 63108, United States.
(Scherrer, True) Research Service, St. Louis VAMC, St. Louis, MO, United States.
(Lyons) Department of Psychology, Boston University, Boston, MA, United States.
(Tsuang) Institute of Behavioral Genomics, Department of Psychiatry, U of California San Diego, San Diego, CA,
United States.
(Tsuang) Harvard Institute of Psychiatric Epidemiology and Genetics, Harvard Departments of Epidemiology and
Psychiatry, Boston, MA, United States.
(True) School of Public Health, Saint Louis University, St. Louis, MO, United States.
Country of Publication
United Kingdom
Title
Subjective reactions to cocaine and marijuana are associated with abuse and
dependence.
Source
Addictive Behaviors. 30(8)(pp 1574-1586), 2005. Date of Publication: Sep 2005.
Abstract
Subjective effects of marijuana and cocaine use are associated with amount of drug use and
potentially with risk of abuse and dependence. We used Latent Class Analyses (LCA) to
examine subjective responses to two categories of drugs and link these to abuse and
dependence. In 1992, subjective responses were queried of 2506 marijuana and 661 cocaine
lifetime users who were members of the Vietnam Era Twin Registry. LCA was used to identify
classes of subjective effects. Multinomial logistic regression models were computed to test for
an association between classes and marijuana and cocaine abuse or dependence. The best
LCA solution for marijuana identified 6 distinct classes characterized as positive, relaxed,
reactive, adverse, low and very reactive. The best LCA solution for cocaine identified 5
distinct classes characterized as positive, alert, adverse, low and very reactive. Marijuana
abuse and dependence were significantly associated with each latent class. Cocaine abuse
was associated with the reactive class (OR = 3.9; 95% CI: 1.6-9.5). Cocaine dependence was
associated with reactive (OR = 15.3; 95% CI: 7.1-32.6), adverse (OR = 9.7; 95% CI: 4.5-21.0)
and very reactive (OR = 18.7; 95% CI: 5.6-62.6) classes. We found evidence for both
qualitative and quantitative subjective effect profiles. Subjective effects, both positive and
adverse are associated with lifetime risk for marijuana and cocaine dependence. copyright
2005 Elsevier Ltd. All rights reserved.
ISSN 0306-4603
Publication Type Journal: Article
Journal Name Addictive Behaviors
Volume 30
Issue Part 8
Page 1574-1586
Year of Publication 2005
Date of Publication Sep 2005
COCAINE (A) <208>
Database EMBASE
Accession Number 2005373097
Authors Hollander J.A. Carelli R.M.
Institution
(Hollander, Carelli) Department of Psychology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United
States.
(Carelli) Department of Psychology, University of North Carolina at Chapel Hill, Davie Hall, Chapel Hill, NC 275993270, United States.
Country of Publication
United Kingdom
Title
Abstinence from cocaine self-administration heightens neural encoding of goaldirected behaviors in the accumbens.
Source
Neuropsychopharmacology. 30(8)(pp 1464-1474), 2005. Date of Publication: Aug 2005.
Abstract
Cocaine addiction in humans is characterized by cycles of abstinence from drug-taking and
relapse. Here, electrophysiological recording procedures were used to determine whether
nucleus accumbens (Acb) neuronal firing properties are altered following interruption and
resumption of cocaine self-administration. Rats (n = 12) were trained to self-administer
cocaine (2 h daily sessions) then divided into two groups. Acb activity was recorded for Group
1 (controls) during two additional self-administration sessions completed over the next 2 days
(test sessions 1 and 2). Acb activity was recorded for Group 2 (1-month) during one selfadministration session completed the next day (test 1), and during a second selfadministration session 1 month later (test 2). As in prior reports, a subset of Acb neurons
exhibited patterned discharges (short duration and/or long-term cyclic alterations, termed
'phasically active') relative to cocaine-reinforced responding during test session 1.
Remarkably, the percentage of phasically active cells dramatically increased (nearly two-fold)
following 1-month abstinence, in the core but not the shell of the Acb. Likewise, the strength
of the neural correlates (determined via signal-to-baseline ratios) also increased as a function
of abstinence. Extinction experiments in another set of rats (n = 12) revealed an increased
motivational state for the drug following abstinence. The results show that abstinence from
cocaine self-administration causes a dramatic increase in the number and strength of Acb
neurons that encode cocaine-related information, thus representing the first
neurophysiological correlate of heightened activation of the 'brain reward system' following
abstinence and resumption (relapse) of cocaine consumption. copyright 2005 Nature
Publishing Group. All rights reserved.
ISSN 0893-133X
Publication Type Journal: Article
Journal Name Neuropsychopharmacology
Volume 30
Issue Part 8
Page 1464-1474
Year of Publication 2005
Date of Publication Aug 2005
COCAINE (A) <209>
Database EMBASE
Accession Number 2005373095
Authors Zhang D. Zhang L. Tang Y. Zhang Q. Lou D. Sharp F.R. Zhang J. Xu M.
Institution
(Zhang, Zhang, Zhang, Lou, Zhang, Xu) Department of Cell Biology, Neurobiology and Anatomy, University of
Cincinnati College of Medicine, Cincinnati, OH 45267-0521, United States.
(Tang, Sharp) Department of Neurology, University of Cincinnati College of Medicine, Cincinnati, OH, United
States.
Country of Publication
United Kingdom
Title
Repeated cocaine administration induces gene expression changes through the
dopamine D1 receptors.
Source
Neuropsychopharmacology. 30(8)(pp 1443-1454), 2005. Date of Publication: Aug 2005.
Abstract
Drug addiction involves compulsive drug-seeking and drug-taking despite known adverse
consequences. The enduring nature of drug addiction suggests that repeated exposure to
abused drugs leads to stable alterations that likely involve changes in gene expression in the
brain. The dopamine D1 receptor has been shown to mediate the long-term behavioral effects
of cocaine. To examine how the persistent behavioral effects of cocaine correlate with
underlying changes in gene expression, we have used D1 receptor mutant and wild-type mice
to identify chronic cocaine-induced gene expression changes mediated via the D1 receptors.
We focused on the caudoputamen and nucleus accumbens, two key brain regions that
mediate the long-term effects of cocaine. Our analyses demonstrate that repeated cocaine
administration induces changes in the expression of 109 genes, including those encoding the
stromal cell-derived factor 1, insulin-like growth factor binding protein 6, sigma 1 receptor,
regulators of G-protein signaling protein 4, Wnt1 responsive Cdc42 homolog,
Ca<sup>2+</sup>/calmodulin- dependent protein kinase II alpha subunit, and cyclin D2, via
the D1 receptors. Moreover, the seven genes contain AP-1 binding sites in their promoter
regions. These results suggest that genes encoding certain extracellular factors, membrane
receptors and modulators, and intracellular signaling molecules, among others, are regulated
by cocaine via the D1 receptor, and these AP-1 transcription complex-regulated genes might
contribute to persistent cocaine-induced behavioral changes. copyright 2005 Nature
Publishing Group. All rights reserved.
ISSN 0893-133X
Publication Type Journal: Article
Journal Name Neuropsychopharmacology
Volume 30
Issue Part 8
Page 1443-1454
Year of Publication 2005
Date of Publication Aug 2005
COCAINE (A) <226>
Database EMBASE
Accession Number 2005340669
Authors Liu Y. Roberts D.C.S. Morgan D.
Institution
(Liu, Roberts, Morgan) Neuroscience Program, Wake Forest University School of Medicine, Winston-Salem, NC
27157, United States.
(Roberts, Morgan) Department of Physiology and Pharmacology, Wake Forest University School of Medicine,
Winston-Salem, NC 27157, United States.
(Morgan) Division of Addiction Medicine, Department of Psychiatry, University of Florida College of Medicine, PO
Box 100183, Gainesville, FL 32610, United States.
Country of Publication
United Kingdom
Title
Sensitization of the reinforcing effects of self-administered cocaine in rats: Effects of
dose and intravenous injection speed.
Source
European Journal of Neuroscience. 22(1)(pp 195-200), 2005. Date of Publication: Jul 2005.
Abstract
Speed of drug onset is assumed to be an important determinant of the abuse liability of a
drug. Studies in human and non-human primates suggest that the subjective and reinforcing
effects of cocaine can be influenced by route of administration and/or speed of intravenous
injection. Sensitization to the reinforcing effects of cocaine was studied in rats and the effects
of various injection durations (i.e. speed of injection) on the development of sensitization was
examined using a progressive ratio schedule. In addition, the effects of cocaine dose on
sensitization and the effects of injection duration on the acute reinforcing effects of cocaine
were examined. The initial study demonstrated that the development of sensitization (i.e.
progressive increases in breakpoints) was dose-dependent. A robust sensitization of the
reinforcing effects of cocaine was replicated in animals receiving cocaine at the highest rate
(i.e. shortest duration; 5 s), but not in animals receiving the same dose over 25 or 50 s.
Subsequent testing revealed that injection duration did not have profound effects on the acute
reinforcing effects of cocaine (assessed by breakpoints or rate of responding on a fixed ratio
schedule). These findings are similar to recent studies demonstrating that the development of
sensitization, but not the acute responsivity, to cocaine's locomotor-activating effects are
influenced by rate of intravenous injection. Taking these findings together, we hypothesize
that the process of drug addiction involves both the acute reinforcing effects and the
development of sensitization. copyright 2005 Federation of European Neuroscience Societies.
ISSN 0953-816X
Publication Type Journal: Article
Journal Name European Journal of Neuroscience
Volume 22
Issue Part 1
Page 195-200
Year of Publication 2005
Date of Publication Jul 2005
COCAINE / VIROLOGY <248>
Database EMBASE
Accession Number 2005316203
Authors Leukefeld C.G. Pechansky F. Martin S.S. Surratt H.L. Inciardi J.A. Kessler F.H.P. Orsi M.M. Von Diemen L.
Meyer Da Silva E.
Institution
(Leukefeld, Meyer Da Silva) University of Kentucky, Lexington, KY, United States.
(Pechansky, Kessler, Orsi, Von Diemen) Federal University of Rio Grande do Sul, Porto Alegre, Brazil.
(Martin, Surratt, Inciardi) University of Delaware, Coral Gables, FL, United States.
(Leukefeld) University of Kentucky, Center on Drug and Alcohol Research, 643 Maxwelton Court, Lexington, KY
40506, United States.
Country of Publication
United Kingdom
Title
Tailoring an HIV-prevention intervention for cocaine injectors and crack users in
Porto Alegre, Brazil.
Source
AIDS Care - Psychological and Socio-Medical Aspects of AIDS/HIV. 17(SUPPL. 1)(pp S77S87), 2005. Date of Publication: 2005.
Abstract
Brazil has the second largest number of reported AIDS cases in the world. Porto Alegre, like
most other large urban centres in Brazil, has been greatly impacted by an AIDS epidemic
driven by high rates of drug use and risky sexual behaviours. While epidemiologic
surveillance of HIV/AIDS and treatment initiatives for HIV-infected individuals are well
developed in Brazil, comparatively little attention has focused on developing interventions
directed toward high-risk populations. Intervention programmes, particularly those tailored for
chronic drug users, are lacking. This pilot project successfully adapted and tailored a
cognitive behavioural HIV intervention developed in the US to the cultural setting in Porto
Alegre. The project established feasibility and acceptability of the approach for targeting risky
drug and sexual behaviours among a group of male Brazilian drug users. A sample of 120
male cocaine users was recruited from a public health clinic serving the target population in
the city of Porto Alegre. The average age of the participants was 29; they averaged less than
8 years of formal education; and less than half (41%) were married. Lifetime self-reported
drug use was high with 93% reporting cocaine use, 87% reporting crack use, and 100%
reporting marijuana use. 43% of the sample reported ever injecting drugs. Reports of risky
sexual behaviours were similarly elevated. Almost half (45%) tested positive for HIV.
Preliminary evidence suggests that intervention acceptability was high among participants.
Given the reported high risk sexual and drug use behaviours among these men, HIV
interventions must be evaluated and expanded to include this population as well as their
sexual partners. copyright 2005 Taylor & Francis Group Ltd.
ISSN 0954-0121
Publication Type Journal: Article
Journal Name AIDS Care - Psychological and Socio-Medical Aspects of AIDS/HIV
Volume 17
Issue Part SUPPL. 1
Page S77-S87
Year of Publication 2005
Date of Publication 2005
COCAINE <270>
Database EMBASE
Accession Number 2005309515
Authors Xi Z.-X. Gilbert J.G. Pak A.C. Ashby Jr. C.R. Heidbreder C.A. Gardner E.L.
Institution
(Xi, Gilbert, Pak, Gardner) Neuropsychopharmacology Section, National Institute on Drug Abuse, National Institutes
of Health, 5500 Nathan Shock Drive, Baltimore, MD 21224, United States.
(Ashby Jr.) Department of Pharmaceutical Sciences, College of Pharmacy and Allied Health Professions, Saint
John's University, Jamaica, NY 11439, United States.
(Heidbreder) Department of Neuropsychopharmacology, Centre of Excellence for Drug Discovery in Psychiatry,
GlaxoSmithKline Pharmaceuticals, 37135 Verona, Italy.
Country of Publication
United Kingdom
Title
Selective dopamine D<sub>3</sub> receptor antagonism by SB-277011A attenuates
cocaine reinforcement as assessed by progressive-ratio and variable-cost-variablepayoff fixed-ratio cocaine self-administration in rats.
Source
European Journal of Neuroscience. 21(12)(pp 3427-3438), 2005. Date of Publication: Jun
2005.
Abstract
In rats, acute administration of SB-277011 A, a highly selective dopamine (DA)
D<sub>3</sub> receptor antagonist, blocks cocaine-enhanced brain stimulation reward,
cocaine-seeking behaviour and reinstatement of cocaine-seeking behaviour. Here, we
investigated whether SB-277011A attenuates cocaine reinforcement as assessed by cocaine
self-administration under variable-cost-variable-payoff fixed-ratio (FR) and progressive-ratio
(PR) reinforcement schedules. Acute i.p. administration of SB-277011 A (3-24 mg/kg) did not
significantly alter cocaine (0.75 mg/kg/infusion) self-administration reinforced under FR1 (one
lever press for one cocaine infusion) conditions. However, acute administration of SB-277011
A (24 mg/kg, i.p.) progressively attenuated cocaine self-administration when: (a) the unit dose
of self-administered cocaine was lowered from 0.75 to 0.125-0.5 mg/kg, and (b) the work
demand for cocaine reinforcement was increased from FR1 to FR10. Under PR (increasing
number of lever presses for each successive cocaine infusion) cocaine reinforcement, acute
administration of SB-277011A (6-24 mg/kg i.p.) lowered the PR break point for cocaine selfadministration in a dose-dependent manner. The reduction in the cocaine (0.25-1.0 mg/kg)
dose-response break-point curve produced by 24 mg/kg SB-277011 A is consistent with a
reduction in cocaine's reinforcing efficacy. When substituted for cocaine, SB-277011A alone
did not sustain self-administration behaviour. In contrast with the mixed DA
D<sub>2</sub>/D<sub>3</sub> receptor antagonist haloperidol (1 mg/kg), SB-277011A (3,
12 or 24 mg/kg) failed to impede locomotor activity, failed to impair rearing behaviour, failed to
produce catalepsy and failed to impair rotarod performance. These results show that SB277011A significantly inhibits acute cocaine-induced reinforcement except at high cocaine
doses and low work requirement for cocaine. If these results extrapolate to humans, SB277011A or similar selective DA D<sub>3</sub> receptor antagonists may be useful in the
treatment of cocaine addiction. copyright 2005 Federation of European Neuroscience
Societies.
ISSN 0953-816X
Publication Type Journal: Article
Journal Name European Journal of Neuroscience
Volume 21
Issue Part 12
Page 3427-3438
Year of Publication 2005
Date of Publication Jun 2005
COCAINE <274>
Database EMBASE
Accession Number 2005300067
Authors Herman B.H. Elkashef A. Vocci F.
Institution
(Herman, Elkashef) Clinical Medical Branch, PMC, NIDA, Bethesda, MD 20892-9551, United States.
(Herman, Elkashef, Vocci) Division of Pharmacotherapies and Medical Consequence of Drug Abuse, National
Institute on Drug Abuse, National Institute of Health, Bethesda, MD 20892-9551, United States.
Country of Publication
United Kingdom
Title
Medications for the treatment of cocaine addiction: Emerging candidates.
Source
Drug Discovery Today: Therapeutic Strategies. 2(1)(pp 87-92), 2005. Date of Publication:
2005.
Abstract
Today, there are promising candidates for the treatment of cocaine addition in humans.
Based upon clinical research, at least three different neurotransmitter systems appear to be
involved in cocaine addition: gamma-aminobutyric acid (GABA), glutamate and dopamine
(DA). Medications that have shown efficacy in placebo-controlled double-blind randomized
controlled trials include: baclofen, topiramate, modafinil, and disulfiram (Phase IIa, singlesite). These medications effect the neurotransmitter brain systems detailed above. Phase IIb
trials are in progress. copyright 2005 Elsevier Ltd. All rights reserved.
ISSN 1740-6773
Publication Type Journal: Article
Journal Name Drug Discovery Today: Therapeutic Strategies
Volume 2
Issue Part 1
Page 87-92
Year of Publication 2005
Date of Publication 2005
COCAINE <275>
Database EMBASE
Accession Number 2005300066
Authors Dackis C.A.
Institution
(Dackis) University of Pennsylvania, Treatment Research Center, 3900 Chestnut Street, Philadelphia, PA 19104,
United States.
Country of Publication
United Kingdom
Title
New treatments for cocaine abuse.
Source
Drug Discovery Today: Therapeutic Strategies. 2(1)(pp 79-86), 2005. Date of Publication:
2005.
Abstract
Effective pharmacotherapies for cocaine dependence have eluded researchers for decades,
despite intensive investigation, but controlled studies have recently identified several
promising candidates that might finally impact the prognosis of this treatment refractory
disorder. Cocaine acutely activates natural reward pathways that become progressively
dysregulated over the course of addiction, leading to abnormal hedonic function and craving,
especially in response to conditioned environmental cues. The acute and chronic effects of
cocaine on reward-related substrates produce distinct clinical phenomena that might respond
to different medications. Pharmacological strategies to block cocaine euphoria, reverse
clinically significant neuroadaptations, improve prefrontal cortical function and dampen cue-
induced craving are reviewed in the context of known neuronal mechanisms and recent
clinical trials. copyright 2005 Elsevier Ltd. All rights reserved.
ISSN 1740-6773
Publication Type Journal: Article
Journal Name Drug Discovery Today: Therapeutic Strategies
Volume 2
Issue Part 1
Page 79-86
Year of Publication 2005
Date of Publication 2005
COCAINE (A) <296>
Database EMBASE
Accession Number 2005283694
Authors Dickerson T.J. Kaufmann G.F. Janda K.D.
Institution
(Janda) Scripps Research Institute, Department of Chemistry, Skaggs Institute for Chemical Biology, 10550 North
Torrey Pines Road, San Diego, CA 92037, United States.
Country of Publication
United Kingdom
Title
Bacteriophage-mediated protein delivery into the central nervous system and its
application in immunopharmacotherapy.
Source
Expert Opinion on Biological Therapy. 5(6)(pp 773-781), 2005. Date of Publication: Jun
2005.
Abstract
Cocaine addiction continues to be a major health and social problem in spite of
governmental efforts devoted towards educating the public in the dangers of illicit drug use. A
variety of pharmacotherapies and psychosocial programmes have been proposed in an effort
to provide a method for allevi-ating the physical and psychological symptoms of cocaine
abuse. Unfortunately, these methods have been met with limited success, illustrating a critical
need for new effective approaches for the treatment of cocaine addiction. The authors have
recently disclosed an alternative cocaine abuse treatment strategy using intranasal
administration of an engineered filamentous bacteriophage displaying cocaine-sequestering
antibodies on its surface. These phage particles are an effective vector for central nervous
system penetration and are capable of binding cocaine, thereby blocking its behavioural
effects in a rodent model. copyright 2005 Ashley Publications Ltd.
ISSN 1471-2598
Publication Type Journal: Review
Journal Name Expert Opinion on Biological Therapy
Volume 5
Issue Part 6
Page 773-781
Year of Publication 2005
Date of Publication Jun 2005
COCAINE <350>
Database EMBASE
Accession Number 2005226463
Authors Hsu R. Taylor J.R. Newton S.S. Alvaro J.D. Haile C. Han G. Hruby V.J. Nestler E.J. Duman R.S.
Institution
(Hsu, Taylor, Newton, Alvaro, Haile, Duman) Center for Genes and Behaviour, Departments of Psychiatry and
Pharmacology, Yale University School of Medicine, New Haven, CT, United States.
(Han, Hruby) University of Arizona, Tucson, AZ, United States.
(Nestler) University of Texas South-western Medical Center, Dallas, TX, United States.
(Duman) 34 Park St, New Haven, CT 06508, United States.
Country of Publication
United Kingdom
Title
Blockade of melanocortin transmission inhibits cocaine reward.
Source
European Journal of Neuroscience. 21(8)(pp 2233-2242), 2005. Date of Publication: Apr
2005.
Abstract
Melanocortins and the melanocortin-4 receptor (MC4-R) are enriched in the nucleus
accumbens, a brain region that has been implicated in the rewarding action of cocaine and
other drugs of abuse. In the present study we use a number of rat behavioral models to show
that infusion of a melanocortin peptide antagonist into the nucleus accumbens blocks the
reinforcing, incentive motivational, and locomotor sensitizing effects of cocaine. We also show
that locomotor responses to repeated cocaine exposure are completely blocked in MC4-R null
mutant mice and reduced in Agouti mice that overexpress an endogenous inhibitor of
melanocortins in the brain. The results also demonstrate that cocaine administration
increases the expression of MC4-R in the nucleus accumbens and striatum, and that MC4-R
is co-localized with prodynorphin in medium spiny neurons in the nucleus accumbens.
Together, these findings indicate that the behavioral actions of cocaine are dependent on
activation of MC4-R, and suggest that upregulation of this receptor by drug exposure may
contribute to sensitization of these behavioral responses. Modulation of cocaine reward is a
novel action of the melanocortin-MC4-R system and could be targeted for the development of
new medications for cocaine addiction. copyright Federation of European Neuroscience
Societies.
ISSN 0953-816X
Publication Type Journal: Article
Journal Name European Journal of Neuroscience
Volume 21
Issue Part 8
Page 2233-2242
Year of Publication 2005
Date of Publication Apr 2005
COCAINE <361>
Database EMBASE
Accession Number 2005222174
Authors Kubler A. Murphy K. Garavan H.
Institution
(Kubler, Murphy, Garavan) Department of Psychology, Institute of Neuroscience, Trinity College Dublin, Dublin,
Ireland.
(Kubler) Institute of Medical Psychology and Behavioural Neurobiology, University of Tubingen, Tubingen,
Germany.
(Garavan) Department of Psychiatry and Behavioural Medicine, Medical College of Wisconsin, Milwaukee, WI,
United States.
Country of Publication
United Kingdom
Title
Cocaine dependence and attention switching within and between verbal and
visuospatial working memory.
Source
European Journal of Neuroscience. 21(7)(pp 1984-1992), 2005. Date of Publication: Apr
2005.
Abstract
Many studies have shown the negative effects of cocaine on neuropsychological and
cognitive performance in drug-dependent individuals, but little is known about the underlying
neuroanatomy of these dysfunctions. The present study addressed attention switching
between items held in working memory (WM) with a task in which subjects were required to
store and update two items held in verbal or visuospatial WM. Attention-switching frequency
varied between trials, thereby allowing us to isolate the switching component of task
performance. Behavioural data revealed that cocaine addicts performed worse than healthy
controls in all tasks. On the visuospatial task addicts performed at chance levels revealing
particular impairment in visuospatial WM. On the verbal task, in which controls and users
could be matched for performance, we identified attenuated responses in prefrontal and
cingulate cortices and in striatal regions, while other areas such as dorsolateral prefrontal
cortex did not differ between healthy controls and users. The results reveal that addiction may
be accompanied by specific rather than ubiquitous hypoactivation in prefrontal and subcortical
areas and suggest a compromised ability in users to control their attention to their thoughts as
might be particularly relevant when required to switch away from drug-related thoughts, and
thus the dysfunction in attention switching may contribute to the maintenance of addiction.
copyright 2005 Federation of European Neuroscience Societies.
ISSN 0953-816X
Publication Type Journal: Article
Journal Name European Journal of Neuroscience
Volume 21
Issue Part 7
Page 1984-1992
Year of Publication 2005
Date of Publication Apr 2005
COCAINE <383>
Database EMBASE
Accession Number 2005194825
Authors Vocci F.J. Elkashef A.
Institution
(Vocci, Elkashef) National Institute on Drug Abuse, National Institutes of Health, Dept. of Health and Human
Services, Bethesda, MD, United States.
(Vocci) Div. Pharmacother./Med. C. D. A., National Institute on Drug Abuse, MSC 9551, 6001 Executive Boulevard,
Bethesda, MD 20892-9551, United States.
Country of Publication
United Kingdom
Title
Pharmacotherapy and other treatments for cocaine abuse and dependence.
Source
Current Opinion in Psychiatry. 18(3)(pp 265-270), 2005. Date of Publication: May 2005.
Abstract
Purpose of review: This review examines progress being made in the treatment of cocaine
abuse and dependence, with a particular focus on pharmacotherapies. Medications with
apparently very different mechanisms of action have been reported to reduce cocaine use in
controlled clinical trials in outpatient settings. This review will summarize the latest findings in
this area. Recent findings: Of all the medications tested to date, disulfiram has demonstrated
the most consistent effect to reduce cocaine use. Several medications have been reported to
reduce cocaine use in double-blind, placebo-controlled clinical trials, namely baclofen,
modafinil, tiagabine, and topiramate. All pharmacotherapy trials in cocaine-dependent
patients include a behavioral therapy that is common to all participants. Consequently, these
pharmacotherapy trials can be considered to evaluate whether the medication is adding to the
effect of the behavioral therapy. Summary: Confirmatory clinical studies are necessary to
replicate the initial efficacy findings for baclofen, modafinil, tiagabine, and topiramate. More
research is needed in both cocaine and cocaine-alcohol dependent populations. Once
confirmatory studies have been carried out, testing of rational medication combinations with
different behavioral therapies is an obvious next step to increase the ability to manage
cocaine dependence. copyright 2005 Lippincott Williams & Wilkins.
ISSN 0951-7367
Publication Type Journal: Review
Journal Name Current Opinion in Psychiatry
Volume 18
Issue Part 3
Page 265-270
Year of Publication 2005
Date of Publication May 2005