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COCAINE 2010 <88>
Database EMBASE
Accession Number 2010261456
Authors Moeller S.J. Maloney T. Parvaz M.A. Alia-Klein N. Woicik P.A. Telang F. Wang G.-J. Volkow N.D. Goldstein
R.Z.
Institution
(Moeller, Maloney) Department of Psychology, University of Michigan, Ann Arbor, MI 48109, United States.
(Moeller, Parvaz, Alia-Klein, Woicik, Wang, Goldstein) Medical Department, Brookhaven National Laboratory,
Upton, NY 11973, United States.
(Parvaz) Department of Biomedical Engineering, Stony Brook University, Stony Brook, NY 11794, United States.
(Telang) Intramural Program, National Institute on Alcohol Abuse and Alcoholism, Bethesda MD 20892, United
States.
(Volkow) Director's Office, National Institute on Drug Abuse, Bethesda, MD 20892, United States.
Country of Publication
United Kingdom
Title
Impaired insight in cocaine addiction: Laboratory evidence and effects on cocaineseeking behaviour.
Source
Brain. 133(5)(pp 1484-1493), 2010. Date of Publication: May 2010.
Publisher
Oxford University Press
Abstract
Neuropsychiatric disorders are often characterized by impaired insight into behaviour. Such
an insight deficit has been suggested, but never directly tested, in drug addiction. Here we
tested for the first time this impaired insight hypothesis in drug addiction, and examined its
potential association with drug-seeking behaviour. We also tested potential modulation of
these effects by cocaine urine status, an individual difference known to impact underlying
cognitive functions and prognosis. Sixteen cocaine addicted individuals testing positive for
cocaine in urine, 26 cocaine addicted individuals testing negative for cocaine in urine, and 23
healthy controls completed a probabilistic choice task that assessed objective preference for
viewing four types of pictures (pleasant, unpleasant, neutral and cocaine). This choice task
concluded by asking subjects to report their most selected picture type; correspondence
between subjects' self-reports with their objective choice behaviour provided our index of
behavioural insight. Results showed that the urine positive cocaine subjects exhibited
impaired insight into their own choice behaviour compared with healthy controls; this same
study group also selected the most cocaine pictures (and fewest pleasant pictures) for
viewing. Importantly, however, it was the urine negative cocaine subjects whose behaviour
was most influenced by insight, such that impaired insight in this subgroup only was
associated with higher cocaine-related choice on the task and more severe actual cocaine
use. These findings suggest that interventions to enhance insight may decrease drug-seeking
behaviour, especially in urine negative cocaine subjects, potentially to improve their longerterm clinical outcomes. copyright The Author (2010). Published by Oxford University Press on
behalf of the Guarantors of Brain. All rights reserved.
ISSN 0006-8950
Publication Type Journal: Article
Journal Name Brain
Volume 133
Issue Part 5
Page 1484-1493
Year of Publication 2010
Date of Publication May 2010
COCAINE 2010 <110>
Database EMBASE
Accession Number 2010280691
Authors Adinoff B. Devous M.D. Williams M.J. Best S.E. Harris T.S. Minhajuddin A. Zielinski T. Cullum M.
Institution
(Adinoff, Williams, Best, Zielinski, Cullum) Department of Psychiatry, University of Texas Southwestern Medical
Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8564, United States.
(Adinoff, Best) VA North Texas Health Care System, Dallas, TX, United States.
(Devous, Harris) Nuclear Medicine Center, Department of Radiology, University of Texas Southwestern Medical
Center, Dallas, TX, United States.
(Minhajuddin) Department of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, TX,
United States.
Country of Publication
United Kingdom
Title
Altered neural cholinergic receptor systems in cocaine-addicted subjects.
Source
Neuropsychopharmacology. 35(7)(pp 1485-1499), 2010. Date of Publication: June 2010.
Publisher
Nature Publishing Group
Abstract
Changes in the brain's cholinergic receptor systems underlie several neuropsychiatric
disorders, including Alzheimer's disease, schizophrenia, and depression. An emerging
preclinical literature also reveals that acetylcoholine may have an important function in
addictive processes, including reward, learning, and memory. This study was designed to
assess alterations in cholinergic receptor systems in limbic regions of abstinent cocaineaddicted subjects compared with healthy controls. On three separate days, 23 1-to 6-week
abstinent, cocaine-(and mostly nicotine-) addicted subjects and 22 sex-, age-, and racematched control subjects were administered the muscarinic and nicotinic cholinergic agonist
physostigmine, the muscarinic antagonist scopolamine, and saline. Regional cerebral blood
flow (rCBF) after each infusion was determined using single photon emission-computed
tomography. Both cholinergic probes induced rCBF changes (p0.005) in relatively distinct,
cholinergic-rich, limbic brain regions. After physostigmine, cocaine-addicted subjects showed
altered rCBF, relative to controls, in limbic regions, including the left hippocampus, left
amygdala, and right insula. Group differences in the right dorsolateral prefrontal cortex,
posterior cingulate, and middle temporal gyrus were also evident. Scopolamine also revealed
group differences in the left hippocampus and right insula as well as the posterior cingulate
and middle temporal gyrus. Cocaine addicted and controls differ in their subcortical, limbic,
and cortical response to cholinergic probes in areas relevant to craving, learning, and
memory. Cholinergic systems may offer a pharmacologic target for cocaine addiction
treatment. copyright 2010 Nature Publishing Group All rights reserved.
ISSN 0893-133X
Publication Type Journal: Article
Journal Name Neuropsychopharmacology
Volume 35
Issue Part 7
Page 1485-1499
Year of Publication 2010
Date of Publication June 2010
COCAINE 2010 <147>
Database EMBASE
Accession Number 2010298938
Authors Ren Z. Sun W.L. Jiao H. Zhang D. Kong H. Wang X. Xu M.
Institution
(Ren, Sun, Jiao, Zhang, Kong, Xu) Department of Anesthesia and Critical Care, The University of Chicago,
Chicago, IL 60637, United States.
(Wang) Wyeth Research, Collegeville, PA 19426, United States.
Country of Publication
United Kingdom
Title
Dopamine D1 and N-methyl-d-aspartate receptors and extracellular signal-regulated
kinase mediate neuronal morphological changes induced by repeated cocaine
administration.
Source
Neuroscience. 168(1)(pp 48-60), 2010. Date of Publication: June 2010.
Publisher
Elsevier Ltd
Abstract
The development of drug addiction involves persistent cellular and molecular changes in the
CNS. The brain dopamine and glutamate systems play key roles in mediating drug-induced
neuroadaptation. Changes in dendritic morphology in medium spiny neurons (MSNs) in the
nucleus accumbens (NAc) and caudate putamen (CPu) accompany drug-induced enduring
behavioral and molecular changes. We have investigated the potential involvement of
dopamine D1 and D2 receptors, the N-methyl-. d-aspartate (NMDA) receptor, and the
extracellular signal-regulated kinase (ERK) in dendritic morphological changes induced by
repeated cocaine administration. We show that either a genetic mutation or pharmacological
blockade of dopamine D1 receptors attenuated cocaine-induced changes in both dendritic
branching and spine density of MSNs in the shell of the NAc and CPu. In contrast,
antagonism of dopamine D2 receptors had no obvious effect on changes in dendritic
branching but had a partial effect on changes in spine density of MSNs in these brain regions
following repeated cocaine injections. Pharmacological inhibition of either NMDA receptors or
ERK attenuated cocaine-induced changes in both dendritic branching and spine density of
MSNs in the shell of the NAc and CPu. These results suggest that dopamine D1 and NMDA
receptors and ERK contribute significantly to neuronal morphological changes induced by
repeated exposure to cocaine. copyright 2010 IBRO.
ISSN 0306-4522
Publication Type Journal: Article
Journal Name Neuroscience
Volume 168
Issue Part 1
Page 48-60
Year of Publication 2010
Date of Publication June 2010
COCAINE <543>
Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)
Unique Identifier 20504138
Status In-Process
Authors Newport K. Coyne P.
Authors Full Name Newport, Kristina. Coyne, Patrick.
Institution
Hospice of Lancaster County, Lancaster, Pennsylvania 17604-4125, USA. [email protected]
Title
Topical cocaine for relief of mucosal pain.
Source
Journal of Pain & Palliative Care Pharmacotherapy. 24(2):149-51, 2010 Jun.
Journal Name
Journal of Pain & Palliative Care Pharmacotherapy
Country of Publication
England
Abstract
Painful mucosal lesions negatively affect quality of life. When located in the oral cavity, they
can cause pain that interferes with speech and swallowing. Acute pain from intra-oral lesions
is difficult to treat with conventional methods such as systemic opioids or viscous lidocaine.
These cases exemplify a safe, fast and effective method for treating painful mouth lesions
that are not responsive to standard treatments. Mr. D and Mr. G had from painful oral lesions
caused by squamous cell carcinoma. Severe pain interfered with their ability to speak and
swallow, resulting in poor nutrition and dehydration. 4% liquid cocaine, self-applied topically to
the open mouth sores, resulted in relief within minutes in both cases. Repeated dosing every
six hours allowed both patients to restart oral nutrition without any reported side effects.
Topical cocaine has not been described for repeated dosing for oral or other mucosal pain.
Potential side effects of mucosal administration include gingival recession and erythematous
lesions. If the recommended topical doses are exceeded, liquid cocaine may be absorbed
systemically causing a stimulant response or addiction. When used appropriately, however,
this intervention can result in a dramatic improvement in quality of life and functional status.
Publication Type Journal Article.
Date of Publication 2010 Jun
Year of Publication 2010
Issue/Part 2
Volume 24
Page 149-51
COCAINE 2010 <648>
Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)
Unique Identifier 20141397
Status MEDLINE
Authors de Los Cobos JP. Sinol N. Banulus E. Batlle F. Tejero A. Trujols J.
Authors Full Name de Los Cobos, Jose Perez. Sinol, Nuria. Banulus, Enrique. Batlle, Francisca. Tejero, Antoni.
Trujols, Joan.
Institution
Unitat de Conductes Addictives, Servei de Psiquiatria, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
Title
Personality traits of cocaine-dependent patients associated with cocaine-positive
baseline urine at hospitalization.
Source
American Journal of Drug & Alcohol Abuse. 36(1):52-6, 2010 Jan.
Journal Name
American Journal of Drug & Alcohol Abuse
Country of Publication
England
Abstract
BACKGROUND: Cocaine abstinence at treatment entry is considered a predictor of good
response in cocaine dependence treatment. Therefore, identification of factors facilitating
pretreatment cocaine abstinence could be useful for developing new therapeutic strategies.
OBJECTIVE: This retrospective chart review study examines the association between
personality traits and cocaine-positive baseline urinalysis (CPB) in cocaine-dependent
inpatients. METHODS: All 107 participants met DSM-IV criteria for cocaine dependence, and
were admitted consecutively to a closed addiction unit for detoxification treatment. Personality
was assessed with the Temperament and Character Inventory and the Millon Clinical
Multiaxial Inventory (MCMI-II). RESULTS: CPB was detected in 80 patients (74.8%). The
logistic regression model solely based on personality dimensions showed that only the MCMIII avoidant traits were significantly associated with a decreased probability of cocainedependent patients presenting CPB. The logistic regression model based on both personality
dimensions and substance use-related variables alike retained the number of days of cocaine
use during the last 30 days as a risk factor, and alcohol dependence and the MCMI-II schizoid
dimension as protective factors in predicting CPB results. CONCLUSION AND SCIENTIFIC
SIGNIFICANCE: Avoidant and schizoid traits are personality dimensions of cocainedependent patients that are associated with cocaine abstinence prior to inpatient admission.
These findings suggest an inverse relationship between social isolation and CPB.
Notwithstanding, more research is needed, not only to assess the generalizability of these
findings, but also to enrich the personality and substance use model with variables related to
readiness to change.
Publication Type Comparative Study. Journal Article. Research Support, Non-U.S. Gov't.
Date of Publication 2010 Jan
Year of Publication 2010
Issue/Part 1
Volume 36
Page 52-6
COCAINE 2010 <654>
Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)
Unique Identifier 19491693
Status MEDLINE
Authors de Millas W. Haasen C. Reimer J. Eiroa-Orosa FJ. Schaefer I.
Authors Full Name de Millas, Walter. Haasen, Christian. Reimer, Jens. Eiroa-Orosa, Francisco Jose. Schaefer,
Ingo.
Institution
Center for Interdisciplinary Addiction Research, Department of Psychiatry, University Medical Center HamburgEppendorf, Hamburg, Germany.
Title
Emergencies related to cocaine use: a European multicentre study of expert
interviews.
Source
European Journal of Emergency Medicine. 17(1):33-6, 2010 Feb.
Journal Name
European Journal of Emergency Medicine
Country of Publication
England
Abstract
Illicit drug use can lead to acute reverse reactions leading to the admission to emergency
departments. Cocaine-related emergencies have been monitored in the USA, but not in
Europe so far. The study investigates patterns of cocaine emergencies in eight European
cities in a multicentre cross-sectional study conducted in Barcelona, Budapest, Dublin,
Hamburg, London, Rome, Vienna and Zurich. The reported frequency differs from city to city,
with some emergency centres having less than one case per half year, and some centres
having more than one case per month. Patterns of complaints among cocaine users are
associated with the psychomotor-stimulant or cardiovascular effects of cocaine. Urine screens
and referrals to the addiction services are infrequent. A closer link between the emergency
departments and addiction services would help in guiding problematic drug users towards
appropriate treatment at an earlier stage in the addiction process.
Publication Type Journal Article. Multicenter Study. Research Support, Non-U.S. Gov't.
Date of Publication 2010 Feb
Year of Publication 2010
Issue/Part 1
Volume 17
Page 33-6
COCAINE 2010 <989>
Database
Ovid MEDLINE(R) Daily Update
Unique Identifier
20030966
Status
MEDLINE
Authors
Caselles A. Mico JC. Amigo S.
Authors Full Name
Caselles, Antonio. Mico, Joan C. Amigo, Salvador.
Institution
Departament de Matematica Aplicada, Universitat de Valencia, Spain. [email protected]
Title
Cocaine addiction and personality: a mathematical model.
Source
British Journal of Mathematical & Statistical Psychology. 63(Pt 2):449-80, 2010 May.
Journal Name
British Journal of Mathematical & Statistical Psychology
Country of Publication
England
Abstract
The existence of a close relation between personality and drug consumption is recognized,
but the corresponding causal connection is not well known. Neither is it well known whether
personality exercises an influence predominantly at the beginning and development of
addiction, nor whether drug consumption produces changes in personality. This paper
presents a dynamic mathematical model of personality and addiction based on the unique
personality trait theory (UPTT) and the general modelling methodology. This model attempts
to integrate personality, the acute effect of drugs, and addiction. The UPTT states the
existence of a unique trait of personality called extraversion, understood as a dimension that
ranges from impulsive behaviour and sensation-seeking (extravert pole) to fearful and
anxious behaviour (introvert pole). As a consequence of drug consumption, the model
provides the main patterns of extraversion dynamics through a system of five coupled
differential equations. It combines genetic extraversion, as a steady state, and dynamic
extraversion in a unique variable measured on the hedonic scale. The dynamics of this
variable describes the effects of stimulant drugs on a short-term time scale (typical of the
acute effect); while its mean time value describes the effects of stimulant drugs on a longterm time scale (typical of the addiction effect). This understanding may help to develop
programmes of prevention and intervention in drug misuse.
ISSN Print 0007-1102
Publication Type Journal Article.
Date of Publication 2010 May
Year of Publication 2010
Issue/Part Pt 2
Volume 63
Page 449-80
COCAINE / AMPHETAMINES 2010 <732>
Database EMBASE
Accession Number 2009650556
Authors Sofuoglu M.
Institution
(Sofuoglu) Yale University, Department of Psychiatry, VA Connecticut Healthcare System, 950 Campbell Avenue,
West Haven, CT 06516, United States.
Country of Publication
United Kingdom
Title
Cognitive enhancement as a pharmacotherapy target for stimulant addiction.
Source
Addiction. 105(1)(pp 38-48), 2010. Date of Publication: January 2010.
Publisher
Blackwell Publishing Ltd
Abstract
Background No medications have been proven to be effective for cocaine and
methamphetamine addiction. Attenuation of drug reward has been the main strategy for
medications development, but this approach has not led to effective treatments. Thus, there is
a need to identify novel treatment targets in addition to the brain reward system. Aim To
propose a novel treatment strategy for stimulant addiction that will focus on medications
enhancing cognitive function and attenuating drug reward. Methods Pre-clinical and clinical
literature on potential use of cognitive enhancers for stimulant addiction pharmacotherapy
was reviewed. Results and conclusions Cocaine and methamphetamine users show
significant cognitive impairments, especially in attention, working memory and response
inhibition functions. The cognitive impairments seem to be predictive of poor treatment
retention and outcome. Medications targeting acetylcholine and norepinephrine are
particularly well suited for enhancing cognitive function in stimulant users. Many cholinergic
and noradrenergic medications are on the market and have a good safety profile and low
abuse potential. These include galantamine, donepezil and rivastigmine (cholinesterase
inhibitors), varenicline (partial nicotine agonist), guanfacine (alpha2-adrenergic agonist) and
atomoxetine (norepinephrine transporter inhibitor). Future clinical studies designed optimally
to measure cognitive function as well as drug use behavior would be needed to test the
efficacy of these cognitive enhancers for stimulant addiction. copyright 2010 Society for the
Study of Addiction.
ISSN 0965-2140
Publication Type Journal: Review
Journal Name Addiction
Volume 105
Issue Part 1
Page 38-48
Year of Publication 2010
Date of Publication January 2010
COCAINE / ECSTASY 2010 <754>
Database EMBASE
Accession Number 2009640171
Authors Alvarenga T.A. Andersen M.L. Ribeiro D.A. Araujo P. Hirotsu C. Costa J.L. Battisti M.C. Tufik S.
Institution
(Alvarenga, Andersen, Araujo, Hirotsu, Battisti, Tufik) Department of Psychobiology, Universidade Federal de Sao
Paulo (UNIFESP), Brazil.
(Ribeiro) Biosciences, Universidade Federal de Sao Paulo (UNIFESP), Brazil.
(Costa) Instrumental Analysis Laboratory, Criminalistic Institute, Brazil.
Country of Publication
United Kingdom
Title
Single exposure to cocaine or ecstasy induces DNA damage in brain and other
organs of mice.
Source
Addiction Biology. 15(1)(pp 96-99), 2010. Date of Publication: January 2010.
Publisher
Blackwell Publishing Ltd
Abstract
We evaluated the overall genetic damage induced by different doses of cocaine and MDMA
(3,4-Methylenedioxymethamphetamine) in several organs. One hour after intraperitoneal drug
administration, mice were euthanized; peripheral blood, liver and brain were collected, and
the cellular suspensions were used for the single cell gel (comet) assay. We determined that
all doses of cocaine and MDMA tested were able to induce DNA damage in blood cells.
Extensive genotoxic damage was induced by cocaine or MDMA at the highest doses used in
liver cells. Brain cells were affected by all doses administrated. These findings demonstrate
that cocaine and MDMA are potent genotoxins. copyright 2009 Society for the Study of
Addiction.
ISSN 1355-6215
Publication Type Journal: Article
Journal Name Addiction Biology
Volume 15
Issue Part 1
Page 96-99
Year of Publication 2010
Date of Publication January 2010
COCAINE (A) 2010 <755>
Database EMBASE
Accession Number 2009640170
Authors Fiancette J.-F. Balado E. Piazza P.-V. Deroche-Gamonet V.
Institution
(Fiancette, Balado, Piazza, Deroche-Gamonet) INSERM U862, NeuroCentre Francois Magendie, Physiopathologie
de la Plasticite Neuronale, 146 rue Leo Saignat, 33077 Bordeaux Cedex, France.
(Fiancette, Balado, Piazza, Deroche-Gamonet) Universite de Bordeaux, Bordeaux, France.
Country of Publication
United Kingdom
Title
Mifepristone and spironolactone differently alter cocaine intravenous selfadministration and cocaine-induced locomotion in C57BL/6J mice.
Source
Addiction Biology. 15(1)(pp 81-87), 2010. Date of Publication: January 2010.
Publisher
Blackwell Publishing Ltd
Abstract
Corticosterone, the main glucorticoid hormone in rodents, facilitates behavioral responses to
cocaine. Corticosterone is proposed to modulate cocaine intravenous self-administration (SA)
and cocaine-induced locomotion through distinct receptors, the glucocorticoid receptor (GR)
and the mineralocorticoid receptor (MR), respectively. However, this remains debatable. On
one hand, modulation of both responses by the GR was tested in different experimental
conditions, i.e. light versus dark nycthemeral phase and naive versus cocaine-experienced
animals. On the other hand, modulation of both responses by the MR was never tested
directly but only inferred based on the ability of low plasma corticosterone levels (those for
which corticosterone almost exclusively binds the MR) to compensate the effects of
adrenalectomy. Our goal here was to test the involvement of the GR and the MR in cocaineinduced locomotor and reinforcing effects in the same experimental conditions. C57Bl/6J mice
were trained for cocaine (1 mg/kg/infusion) intravenous SA over 40 SA sessions. The animals
were then administered with mifepristone (30 mg/kg i.p.), a GR antagonist, or with
spironolactone (20 mg/kg/i.p.), an MR antagonist, 2 hours before either cocaine intravenous
SA or cocaine-induced locomotion. In a comparable nycthemeral period and in similarly
cocaine-experienced animals, a blockade of the GR decreased cocaine-induced reinforcing
effects but not cocaine-induced locomotion. A blockade of the MR decreased both cocaineinduced reinforcing (but to a much lesser extent than the GR blockade) and locomotor effects.
Altogether, our results comforted the hypothesis that the GR modulates cocaine-related
operant conditioning, while the MR would modulate cocaine-related unconditioned effects.
The present data also reveal mifepristone as an interesting tool for manipulating the impact of
corticosterone on cocaine-induced reinforcing effects in mice. copyright 2009 Society for the
Study of Addiction.
ISSN 1355-6215
Publication Type Journal: Article
Journal Name Addiction Biology
Volume 15
Issue Part 1
Page 81-87
Year of Publication 2010
Date of Publication January 2010
COCAINE (A) 2010 <784>
Database EMBASE
Accession Number 2009627141
Authors Rodriguez-Borrero E. Rivera-Escalera F. Candelas F. Montalvo J. Munoz-Miranda W.J. Walker J.R.
Maldonado-Vlaar C.S.
Institution
(Rodriguez-Borrero, Rivera-Escalera, Candelas, Montalvo, Munoz-Miranda, Maldonado-Vlaar) University of Puerto
Rico, Department of Biology, P.O. Box 23360, San Juan, PR 00931, United States.
(Walker) Novartis Genome Institute, San Diego, CA, United States.
Country of Publication
United Kingdom
Title
Arginine vasopressin gene expression changes within the nucleus accumbens during
environment elicited cocaine-conditioned response in rats.
Source
Neuropharmacology. 58(1)(pp 88-101), 2010. Date of Publication: January 2010.
Publisher
Elsevier Ltd
Abstract
It is known that changes in gene expression within the nucleus accumbens (NAc) occur
during cocaine dependence development. However, identification of specific genes involved
in cocaine conditioning awaits further investigation. We conducted a high throughput gene
expression profile analysis of the NAc, during different stages of the environment-elicited
cocaine conditioning. Rats were assigned to two different environmental conditions. Cocaine
conditioned group received a cocaine injection (10 mg/kg, i.p.) prior to being placed in the
activity chambers. Control rats received saline injections before being exposed to their
environment. Both groups received a saline injection in their home cage. Conditioning training
lasted for 10 days. Animals were then re-exposed to their previously paired environments only
on day 12 (test session). We found that the gene for arginine vasopressin (AVP) was
differentially expressed on experimental subjects during all stages of environment-elicited
cocaine conditioning. To further validate our molecular results, biochemical and
immunolocalization experiments were conducted. We found the presence of AVP within
accumbal fibers and changes in AVP protein levels following cocaine conditioning. Moreover,
we tested the effects of accumbal microinfusions of either AVP receptor V1A agonist [pGlu4,
Cyt6, Arg8] AVP 4-9 1.0 ng/0.5 mul, or V1A antagonist (CH2) 5[Tyr (Me) 2] AVP, 1.0 ng/0.5
mul or vehicle solution (0.9% saline solution) during different stages of the cocaine
conditioning. Blockade of V1A receptors within the NAc during acquisition interrupted the
expression of the conditioned response, while activation leads to an increase in this response.
Our findings propose a new role for AVP in cocaine addiction. copyright 2009 Elsevier Ltd. All
rights reserved.
ISSN 0028-3908
Publication Type Journal: Article
Journal Name Neuropharmacology
Volume 58
Issue Part 1
Page 88-101
Year of Publication 2010
Date of Publication January 2010
COCAINE 2010 <785>
Database EMBASE
Accession Number 2009627138
Authors Smith R.J. Tahsili-Fahadan P. Aston-Jones G.
Institution
(Smith, Tahsili-Fahadan, Aston-Jones) Department of Neurosciences, Medical University of South Carolina, 173
Ashley Ave., 403 Basic Science Bldg, Charleston, SC 29425-5100, United States.
Country of Publication
United Kingdom
Title
Orexin/hypocretin is necessary for context-driven cocaine-seeking.
Source
Neuropharmacology. 58(1)(pp 179-184), 2010. Date of Publication: January 2010.
Publisher
Elsevier Ltd
Abstract
Orexin/hypocretin signaling at the orexin 1 receptor (OX1R) has recently been implicated in
addiction and relapse. We examined the role of the orexin system in cocaine-seeking elicited
by a drug-associated context following abstinence or extinction from chronic cocaine selfadministration. Male Sprague-Dawley rats self-administered cocaine in 2-h sessions for 10
days, followed by extinction training or extended abstinence in the home cage. The OX1R
antagonist SB-334867 (SB; 10, 20, or 30 mg/kg, i.p.) was administered prior to re-exposure to
the cocaine self-administration environment. We found that pretreatment with SB significantly
attenuated cocaine-seeking when rats were placed back into the self-administration
environment following either 1 day or 2 weeks of abstinence (no extinction), or following
extinction of cocaine-seeking in an alternative environment (distinct from the training
environment). These results indicate that orexin signaling at OX1R is critical for conditioned
cocaine-seeking elicited by a drug-associated context, following either extinction or
abstinence. copyright 2009 Elsevier Ltd. All rights reserved.
ISSN 0028-3908
Publication Type Journal: Article
Journal Name Neuropharmacology
Volume 58
Issue Part 1
Page 179-184
Year of Publication 2010
Date of Publication January 2010
COCAINE (A) 2010 <787>
Database EMBASE
Accession Number 2009627126
Authors Xi Z.-X. Kiyatkin M. Li X. Peng X.-Q. Wiggins A. Spiller K. Li J. Gardner E.L.
Institution
(Xi, Kiyatkin, Li, Peng, Wiggins, Spiller, Li, Gardner) Intramural Research Program, National Institute on Drug
Abuse, Baltimore, MD 21224, United States.
Country of Publication
United Kingdom
Title
N-acetylaspartylglutamate (NAAG) inhibits intravenous cocaine self-administration
and cocaine-enhanced brain-stimulation reward in rats.
Source
Neuropharmacology. 58(1)(pp 304-313), 2010. Date of Publication: January 2010.
Publisher
Elsevier Ltd
Abstract
Pharmacological activation of group II metabotropic glutamate (mGlu2 and mGlu3) receptors
inhibits reward-seeking behavior and/or rewarding efficacy induced by drugs (cocaine,
nicotine) or natural rewards (food, sucrose). In the present study, we investigated whether
elevation of brain N-acetylaspartylglutamate (NAAG), an endogenous group II mGlu receptor
agonist, by the NAAG peptidase inhibitor 2-PMPA attenuates cocaine's rewarding effects, as
assessed by intravenous cocaine self-administration and intracranial electrical brainstimulation reward (BSR) in rats. Systemic administration of 2-PMPA (10, 30, 100 mg/kg, i.p.)
or intranasal administration of NAAG (100, 300 mug/10 mul/nostril) significantly inhibited
intravenous cocaine self-administration under progressive-ratio (PR), but not under fixed-ratio
2 (FR2), reinforcement conditions. In addition, 2-PMPA (1, 10, 30 mg/kg, i.p) or NAAG (50,
100 mug/10 mul/nostril) significantly inhibited cocaine-enhanced BSR, but not basal BSR.
Pretreatment with LY341495 (1 mg/kg, i.p.), a selective mGlu2/3 receptor antagonist,
prevented the inhibitory effects produced by 2-PMPA or NAAG in both the self-administration
and BSR paradigms. In vivo microdialysis demonstrated that 2-PMPA (10, 30, 100 mg/kg)
dose-dependently attenuated cocaine-enhanced extracellular dopamine (DA) in the nucleus
accumbens (NAc). 2-PMPA alone inhibited basal NAc DA release, an effect that was
prevented by LY341495. These findings suggest that systemic administration of 2-PMPA or
intranasal administration of NAAG inhibits cocaine's rewarding efficacy and cocaineenhanced NAc DA - likely by activation of presynaptic mGlu2/3 receptors in the NAc. These
data suggest a potential utility for 2-PMPA or NAAG in the treatment of cocaine addiction.
ISSN 0028-3908
Publication Type Journal: Article
Journal Name Neuropharmacology
Volume 58
Issue Part 1
Page 304-313
Year of Publication 2010
Date of Publication January 2010
COCAINE 2010 <804>
Database EMBASE
Accession Number 2009627911
Authors Grakalic I. Panlilio L.V. Quiroz C. Schindler C.W.
Institution
(Grakalic, Panlilio, Quiroz, Schindler) DHHS, NIH, NIDA Intramural Research Program, Baltimore, MD, United
States.
Country of Publication
United Kingdom
Title
Effects of orbitofrontal cortex lesions on cocaine self-administration.
Source
Neuroscience. 165(2)(pp 313-324), 2010. Date of Publication: 20 Jan 2010.
Publisher
Elsevier Ltd
Abstract
Previous research has implicated limbic and prefrontal cortical areas in the control of drugseeking behavior. The present study examined the effects of orbitofrontal-cortex (OFC)
lesions on acquisition, dose-dependence, within-session patterning, and reinstatement of
cocaine self-administration. Rats received OFC or sham lesions before or after acquisition
(0.3 mg/kg/injection, paired with a visual stimulus), then were tested with a range of doses (0,
0.03, 0.1, 0.3 and 1). Compared to controls, rats lesioned before acquisition acquired the
behavior sooner, responded more at low doses, and responded more on the first day of
extinction. Rats that were lesioned after acquisition showed an even larger increase in
responding ([similar to]250%) at the lowest dose, and they also showed increased timeout
responding and drug "loading" at low doses. Pre-acquisition lesions were tested and found to
have no effect on cocaine-induced reinstatement. In parallel experiments examining effects of
pre-acquisition OFC lesions on food-reinforced responding, lesions did not alter acquisition,
maintenance, or reinstatement, but accelerated the course of extinction. The increased
cocaine self-administration seen in OFC-lesioned rats did not resemble the dysregulated drug
intake observed in long-access models of addiction but might be due to impaired response
inhibition or impaired tracking of the reward value of drug-related cues.
ISSN 0306-4522
Publication Type Journal: Article
Journal Name Neuroscience
Volume 165
Issue Part 2
Page 313-324
Year of Publication 2010
Date of Publication 20 Jan 2010
COCAINE 2010 <853>
Database EMBASE
Accession Number 2010051720
Authors Espana R.A. Oleson E.B. Locke J.L. Brookshire B.R. Roberts D.C.S. Jones S.R.
Institution
(Espana, Oleson, Locke, Brookshire, Roberts, Jones) Department of Physiology and Pharmacology, Wake Forest
University Health Sciences, Medical Center Boulevard, Winston-Salem, NC 27157, United States.
Country of Publication
United Kingdom
Title
The hypocretin-orexin system regulates cocaine self-administration via actions on the
mesolimbic dopamine system.
Source
European Journal of Neuroscience. 31(2)(pp 336-348), 2010. Date of Publication: January
2010.
Publisher
Blackwell Publishing Ltd
Abstract
Recent evidence suggests that the hypocretin-orexin system participates in the regulation of
reinforcement processes. The current studies examined the extent to which hypocretin
neurotransmission regulates behavioral and neurochemical responses to cocaine, and
behavioral responses to food reinforcement. These studies used a combination of fixed ratio,
discrete trials, progressive ratio and threshold self-administration procedures to assess
whether the hypocretin 1 receptor antagonist, SB-334867, reduces cocaine selfadministration in rats. Progressive ratio sucrose self-administration procedures were also
used to assess the extent to which SB-334867 reduces responding to a natural reinforcer in
food-restricted and food-sated rats. Additionally, these studies used microdialysis and in vivo
voltammetry in rats to examine whether SB-334867 attenuates the effects of cocaine on
dopamine signaling within the nucleus accumbens core. Furthermore, in vitro voltammetry
was used to examine whether hypocretin knockout mice display attenuated dopamine
responses to cocaine. Results indicate that when SB-334867 was administered peripherally
or within the ventral tegmental area, it reduced the motivation to self-administer cocaine and
attenuated cocaine-induced enhancement of dopamine signaling. SB-334867 also reduced
the motivation to self-administer sucrose in food-sated but not food-restricted rats. Finally,
hypocretin knockout mice displayed altered baseline dopamine signaling and reduced
dopamine responses to cocaine. Combined, these studies suggest that hypocretin
neurotransmission participates in reinforcement processes, likely through modulation of the
mesolimbic dopamine system. Additionally, the current observations suggest that the
hypocretin system may provide a target for pharmacotherapies to treat cocaine addiction.
copyright 2010 Federation of European Neuroscience Societies and Blackwell Publishing Ltd.
ISSN 0953-816X
Publication Type Journal: Article
Journal Name European Journal of Neuroscience
Volume 31
Issue Part 2
Page 336-348
Year of Publication 2010
Date of Publication January 2010
COCAINE 2010 <871>
Database EMBASE
Accession Number 2010077310
Authors Tannu N.S. Howell L.L. Hemby S.E.
Institution
(Tannu, Hemby) Department of Physiology and Pharmacology, Wake Forest University School of Medicine,
Winston-Salem, NC 27157, United States.
(Howell) Neuroscience Division, Yerkes National Primate Research Center, Emory University, Atlanta, GA, United
States.
(Howell) Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA,
United States.
(Hemby) Department of Psychiatry and Behavioral Medicine, Wake Forest University School of Medicine, WinstonSalem, NC, United States.
Country of Publication
United Kingdom
Title
Integrative proteomic analysis of the nucleus accumbens in rhesus monkeys
following cocaine self-administration.
Source
Molecular Psychiatry. 15(2)(pp 185-203), 2010. Date of Publication: January 2010.
Publisher
Nature Publishing Group
Abstract
The reinforcing effects and long-term consequences of cocaine self-administration have
been associated with brain regions of the mesolimbic dopamine pathway, namely the nucleus
accumbens (NAc). Studies of cocaine-induced biochemical adaptations in rodent models
have advanced our knowledge; however, unbiased detailed assessments of intracellular
alterations in the primate brain are scarce, yet essential, to develop a comprehensive
understanding of cocaine addiction. To this end, two-dimensional difference in gel
electrophoresis (2D-DIGE) was used to compare changes in cytosolic protein abundance in
the NAc between rhesus monkeys self-administering cocaine and controls. Following image
normalization, spots with significantly differential image intensities (P<0.05) were identified,
excised, trypsin digested and analyzed by matrix-assisted laser-desorption ionization time-offlight time-of-flight (MALDI-TOF-TOF). In total, 1098 spots were subjected to statistical
analysis with 22 spots found to be differentially abundant of which 18 proteins were positively
identified by mass spectrometry. In addition, approximately 1000 protein spots were
constitutively expressed of which 21 proteins were positively identified by mass spectrometry.
proteins in the cocaine-exposed monkeys include glial fibrillary acidic protein, syntaxinbinding protein 3, protein kinase C isoform, adenylate kinase isoenzyme 5 and mitochondrialrelated proteins, whereas decreased levels of proteins included B-soluble N-ethylmaleimidesensitive factor attachment protein and neural and non-neural enolase. Using a
complimentary proteomics approach, the differential expression of phosphorylated proteins in
the cytosolic fraction of these subjects was examined. Two-dimensional gel electrophoresis
(2DGE) was followed by gel staining with Pro-Q Diamond phosphoprotein gel stain, enabling
differentiation of approximately 150 phosphoprotein spots between the groups. Following
excision and trypsin digestions, MALDI-TOF-TOF was used to confirm the identity of 15
cocaine-altered phosphoproteins. Significant increased levels were detected for gammaaminobutyric acid type A receptor-associated protein 1, 14-3-3 gamma-protein, glutathione Stransferase and brain-type aldolase, whereas significant decreases were observed for Bactin, Rab GDP-dissociation inhibitor, guanine deaminase, peroxiredoxin 2 isoform b and
several mitochondrial proteins. Results from these studies indicate coordinated dysregulation
of proteins related to cell structure, signaling, metabolism and mitochondrial function. These
data extend and compliment previous studies of cocaine-induced biochemical alterations in
human postmortem brain tissue, using an animal model that closely recapitulates the human
condition and provide new insight into the molecular basis of the disease and potential targets
for pharmacotherapeutic intervention. copyright 2010 Nature Publishing Group All rights
reserved.
ISSN 1359-4184
Publication Type Journal: Article
Journal Name Molecular Psychiatry
Volume 15
Issue Part 2
Page 185-203
Year of Publication 2010
Date of Publication January 2010
COCAINE 2010 <937>
Database EMBASE
Accession Number 2010113003
Authors Wang L. Lv Z. Hu Z. Sheng J. Hui B. Sun J. Ma L.
Institution
(Wang, Lv, Hu, Sheng, Hui, Sun, Ma) Pharmacology Research Center, Shanghai Medical College, Fudan
University, 138 Yixueyuan Road, Shanghai, Shanghai 200032, China.
Country of Publication
United Kingdom
Title
Chronic cocaine-induced H3 acetylation and transcriptional activation of CaMKIIalpha
in the nucleus accumbens is critical for motivation for drug reinforcement.
Source
Neuropsychopharmacology. 35(4)(pp 913-928), 2010. Date of Publication: March 2010.
Publisher
Nature Publishing Group
Abstract
The regulation of gene expression in the brain reward regions is known to contribute to the
pathogenesis and persistence of drug addiction. Increasing evidence suggests that the
regulation of gene transcription is mediated by epigenetic mechanisms that alter the
chromatin structure at specific gene promoters. To better understand the involvement of
epigenetic regulation in drug reinforcement properties, rats were subjected to cocaine selfadministration paradigm. Daily histone deacetylase (HDAC) inhibitor infusions in the shell of
the nucleus accumbens (NAc) caused an upward shift in the dose-response curve under
fixed-ratio schedule and increased the break point under progressive-ratio schedule,
indicating enhanced motivation for self-administered drug. The effect of the HDAC inhibitor is
attributed to the increased elevation of histone acetylation induced by chronic, but not acute,
cocaine experience. In contrast, neutralizing the chronic cocaine-induced increase in histone
modification by the bilateral overexpression of HDAC4 in the NAc shell reduced drug
motivation. The association between the motivation for cocaine and the transcriptional
activation of addiction-related genes by H3 acetylation in the NAc shell was analyzed. Among
the genes activated by chronic cocaine experiences, the expression of CaMKIIalpha, but not
CaMKIIB, correlated positively with motivation for the drug. Lentivirus-mediated shRNA
knockdown experiments showed that CaMKIIalpha, but not CaMKIIB, in the NAc shell is
essential for the maintenance of motivation to self-administered cocaine. These findings
suggest that chronic drug-use-induced transcriptional activation of genes, such as
CaMKIIalpha, modulated by H3 acetylation in the NAc is a critical regulatory mechanism
underlying motivation for drug reinforcement. copyright 2010 Nature Publishing Group All
rights reserved.
ISSN 0893-133X
Publication Type Journal: Article
Journal Name Neuropsychopharmacology
Volume 35
Issue Part 4
Page 913-928
Year of Publication 2010
Date of Publication March 2010
COCAINE / OPIOIDS 2010 <991>
Database EMBASE
Accession Number 2010123969
Authors McCance-Katz E.F. Jatlow P. Rainey P.M.
Institution
(McCance-Katz) Department of Psychiatry, University of California San Francisco, San Francisco, CA, United
States.
(Jatlow) Department of Laboratory Medicine, Yale University, New Haven, CT, United States.
(Rainey) Department of Laboratory Medicine, University of Washington, Seattle, WA, United States.
(McCance-Katz) San Francisco General Hospital, 1001 Potrero Ave., San Francisco, CA 94110, United States.
Country of Publication
United Kingdom
Title
Effect of cocaine use on methadone pharmacokinetics in humans.
Source
American Journal on Addictions. 19(1)(pp 47-52), 2010. Date of Publication: January February 2010.
Publisher
Wiley-Blackwell
Abstract
Chronic cocaine use has been shown to significantly decrease buprenorphine
concentrations in the blood with potential for adverse events and poor treatment response. In
this study, we investigated whether a similar drug interaction occurred between cocaine and
methadone. In a retrospective analysis, methadone pharmacokinetics were compared for
those who were either regular cocaine users (N = 16) or with intermittent or no cocaine use (N
= 23). Participants who used cocaine regularly showed a significant decrease in Cmin (p
=.04) and a trend for decreased AUC (p =.09) and more rapid methadone clearance (p =.08).
Regular cocaine use may adversely impact treatment outcomes for opioid dependence in
those receiving methadone maintenance by decreasing methadone exposure. copyright
American Academy of Addiction Psychiatry.
ISSN 1055-0496
Publication Type Journal: Article
Journal Name American Journal on Addictions
Volume 19
Issue Part 1
Page 47-52
Year of Publication 2010
Date of Publication January - February 2010
COCAINE / OPIOIDS 2010 <1000>
Database
EMBASE
Accession Number
2010123958
Authors
McCance-Katz E.F. Rainey P.M. Moody D.E.
Institution
(McCance-Katz) Department of Psychiatry, University of California San Francisco, San Francisco, CA, United
States.
(Rainey) Department of Laboratory Medicine, University of Washington, Seattle, WA, United States.
(Moody) Center for Human Toxicology, University of Utah, Salt Lake City, UT, United States.
(McCance-Katz) San Francisco General Hospital, 1001 Potrero Ave., San Francisco, CA 94110, United States.
Country of Publication
United Kingdom
Title
Effect of cocaine use on buprenorphine pharmacokinetics in humans.
Source
American Journal on Addictions. 19(1)(pp 38-46), 2010. Date of Publication: January February 2010.
Publisher
Wiley-Blackwell
Abstract
The effect of chronic cocaine use on buprenorphine pharmacokinetics was investigated to
identify drug interactions and potential toxicities. In a retrospective analysis, pharmacokinetics
were compared for 16 studies completed on subjects who were regular cocaine users and 74
studies on subjects who used cocaine only occasionally or not at all. All participants were
stably maintained on buprenorphine/naloxone 16/4 mg daily. Participants who used cocaine
regularly had lower buprenorphine exposure (AUC 34% lower; Cmax 27% lower and C24
37% lower; p [less-than or equal to].001 for all comparisons). Regular cocaine users were
younger (p =.0007), and used more heroin (p =.004) and cocaine (p <.0001). Regular cocaine
use may result in lower buprenorphine plasma concentrations with potential for adverse
clinical outcomes. copyright American Academy of Addiction Psychiatry.
ISSN 1055-0496
Publication TypeJournal: Article
Journal Name American Journal on Addictions
Volume 19
Issue Part 1
Page 38-46
Year of Publication 2010
Date of Publication January - February 2010