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NEURO 2009 <205>
Database EMBASE
Accession Number 2009000488
Authors Wheeler R.A. Carelli R.M.
Institution
(Wheeler, Carelli) Department of Psychology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599,
United States.
(Carelli) Neuroscience Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States.
Country of Publication
United Kingdom
Title
Dissecting motivational circuitry to understand substance abuse.
Source
Neuropharmacology. 56(SUPPL. 1)(pp 149-159), 2009. Date of Publication: 2009.
Publisher
Elsevier Ltd
Abstract
An important goal of cocaine addiction research is to understand the neurobiological
mechanisms underlying this disease state. Here, we review studies from our laboratory that
examined nucleus accumbens (NAc) cell firing and rapid dopamine signaling using
electrophysiological and electrochemical recordings in behaving rodents. A major advantage
of these techniques is that they allow for the characterization of NAc activity and rapid
dopamine release during specific phases of motivated behavior. Moreover, each approach
enables an examination of the dynamic nature of NAc signaling as a function of factors such
as hedonics and associative learning. We show that NAc neurons differentially respond to
rewarding and aversive stimuli and their predictors in a bivalent manner. This differential
responding is modifiable and can be altered by the presentation of other natural rewards or
cocaine. Likewise, the dynamic nature of NAc cell firing is also reflected in the differential
activation of distinct populations of NAc neurons during goal-directed behaviors for natural
versus drug rewards, and the heightened activation of some NAc neurons following cocaine
abstinence. Our electrochemical data also show that rapid dopamine signaling in the NAc
reflects primary rewards and their predictors and appears to modulate specific NAc neuronal
responses. In some cases, these influences are observed in a regionally specific manner that
matches previous pharmacological manipulations. Collectively, these findings provide critical
insight into the functional organization of the NAc that can be used to guide additional studies
aimed at dissecting the neural code underlying compulsive drug-seeking behavior. copyright
2008 Elsevier Ltd. All rights reserved.
ISSN 0028-3908
Publication Type Journal: Review
Journal Name Neuropharmacology
Volume 56
Issue Part SUPPL. 1
Page 149-159
Year of Publication 2009
Date of Publication 2009
NEURO 2009 <206>
Database EMBASE
Accession Number 2009000483
Authors Volkow N.D. Fowler J.S. Wang G.J. Baler R. Telang F.
Institution
(Volkow, Fowler, Wang, Baler, Telang) National Institute on Drug Abuse, NIH, Bethesda, MD 20892, United States.
Country of Publication
United Kingdom
Title
Imaging dopamine's role in drug abuse and addiction.
Source
Neuropharmacology. 56(SUPPL. 1)(pp 3-8), 2009. Date of Publication: 2009.
Publisher
Elsevier Ltd
Abstract
Dopamine is involved in drug reinforcement but its role in addiction is less clear. Here we
describe PET imaging studies that investigate dopamine's involvement in drug abuse in the
human brain. In humans the reinforcing effects of drugs are associated with large and fast
increases in extracellular dopamine, which mimic those induced by physiological dopamine
cell firing but are more intense and protracted. Since dopamine cells fire in response to salient
stimuli, supraphysiological activation by drugs is experienced as highly salient (driving
attention, arousal, conditioned learning and motivation) and with repeated drug use may raise
the thresholds required for dopamine cell activation and signaling. Indeed, imaging studies
show that drug abusers have marked decreases in dopamine D2 receptors and in dopamine
release. This decrease in dopamine function is associated with reduced regional activity in
orbitofrontal cortex (involved in salience attribution; its disruption results in compulsive
behaviors), cingulate gyrus (involved in inhibitory control; its disruption results in impulsivity)
and dorsolateral prefrontal cortex (involved in executive function; its disruption results in
impaired regulation of intentional actions). In parallel, conditioning triggered by drugs leads to
enhanced dopamine signaling when exposed to conditioned cues, which then drives the
motivation to procure the drug in part by activation of prefrontal and striatal regions. These
findings implicate deficits in dopamine activity-inked with prefrontal and striatal deregulation-in
the loss of control and compulsive drug intake that results when the addicted person takes the
drugs or is exposed to conditioned cues. The decreased dopamine function in addicted
individuals also reduces their sensitivity to natural reinforcers. Therapeutic interventions
aimed at restoring brain dopaminergic tone and activity of cortical projection regions could
improve prefrontal function, enhance inhibitory control and interfere with impulsivity and
compulsive drug administration while helping to motivate the addicted person to engage in
non-drug related behaviors.
ISSN 0028-3908
Publication Type Journal: Review
Journal Name Neuropharmacology
Volume 56
Issue Part SUPPL. 1
Page 3-8
Year of Publication 2009
Date of Publication 2009
NEURO (A) 2009 <217>
Database EMBASE
Accession Number 2009001089
Authors Fonck C. Nashmi R. Salas R. Zhou C. Huang Q. De Biasi M. Lester R.A.J. Lester H.A.
Institution
(Fonck, Zhou, Huang, Lester) Division of Biology, California Institute of Technology, Pasadena, CA 91125, United
States.
(Nashmi) Department of Biology, University of Victoria, BC V8W 3N5, Canada.
(Salas, De Biasi) Department of Neuroscience, Baylor College of Medicine, Houston, TX 77030, United States.
(Lester) Department of Neurobiology, Evelyn F. McKnight Brain Institute, University of Alabama at Birmingham,
1825 University Boulevard, Birmingham, AL 35294-2182, United States.
Country of Publication
United Kingdom
Title
Demonstration of functional alpha4-containing nicotinic receptors in the medial
habenula.
Source
Neuropharmacology. 56(1)(pp 247-253), 2009. Date of Publication: January 2009.
Publisher
Elsevier Ltd
Abstract
The medial habenula (MHb) exhibits exceptionally high levels of nicotinic acetylcholine
receptors (nAChRs), but it remains unclear whether all expressed nAChR subunit mRNAs are
translated to form functional receptors. In particular alpha4 subunits have not been reported
to have any functional role, despite strong alpha4 mRNA expression in the ventrolateral MHb.
We studied a strain of knock-in mice expressing fluorescent alpha4* nAChRs (alpha4YFP), as
well as a knock-in strain expressing hypersensitive alpha4* nAChRs (alpha4L9'A). In
alpha4YFP mice, there was strong fluorescence in the ventrolateral MHb. In hypersensitive
alpha4L9'A mice, injections of a low dose of nicotine (0.1 mg/kg) led to strong c-fos
expression in only the ventrolateral region of the MHb, but not in the MHb of wild-type (WT)
mice. In MHb slice recordings, ventrolateral neurons from alpha4L9'A mice, but not from WT
mice, responded robustly to nicotine (1 muM). Neurons in the medial aspect of the MHb had
>10-fold smaller responses. Thus alpha4* nAChRs contribute to the selective activation of a
subset of MHb neurons. Subunit composition analysis based on gain-of-function knock-in
mice provides a useful experimental paradigm. copyright 2008 Elsevier Ltd. All rights
reserved.
ISSN 0028-3908
Publication Type Journal: Article
Journal Name Neuropharmacology
Volume 56
Issue Part 1
Page 247-253
Year of Publication 2009
Date of Publication January 2009
NEURO 2009 <219>
Database EMBASE
Accession Number 2008607441
Authors Lambe E.K. George T.P.
Institution
(Lambe) Department of Physiology, Department of Obstetrics and Gynecology, University of Toronto, Toronto, ON,
Canada.
(George) Schizophrenia and Addictions Programs, Centre for Addiction and Mental Health (CAMH), Toronto, ON,
Canada.
(George) Departments of Psychiatry and Psychology, University of Toronto, Toronto, ON, Canada.
(Lambe) Department of Physiology, University of Toronto, 1 King's College Circle, Toronto, ON M5S 1A8, Canada.
Country of Publication
United Kingdom
Title
Perspective: Translational studies on glutamate and dopamine neurocircuitry in
addictions: Implications for addiction treatment.
Source
Neuropsychopharmacology. 34(2)(pp 255-256), 2009. Date of Publication: January 2009.
Publisher
Nature Publishing Group
Abstract
New research suggests that the modulation of dopamine neurocircuitry by glutamate plays a
key role in the development of nicotine and other addictions. For example, manipulation of
glutamatergic pathways can alter the mood-enhancing and reinforcing properties of nicotine.
These glutamatergic pathways are also sensitive to manipulation by other drugs of abuse.
The studies described in this special issue of Neuropsychopharmacology bring together
rodent studies with translational work in humans to enhance our understanding of the cellular
mechanisms underlying the subjective and objective effects of drugs of abuse. These studies
suggest new therapeutic targets based on central glutamate systems that may lead to the
development of novel and more effective treatments for addictive disorders. copyright 2009
Nature Publishing Group All rights reserved.
ISSN 0893-133X
Publication Type Journal: Short Survey
Journal Name Neuropsychopharmacology
Volume 34
Issue Part 2
Page 255-256
Year of Publication 2009
Date of Publication January 2009
NEURO 2009 <232>
Database EMBASE
Accession Number 2009025783
Authors Abbracchio M.P. Burnstock G. Verkhratsky A. Zimmermann H.
Institution
(Abbracchio) Department of Pharmacological Sciences, Laboratory of Molecular and Cellular Pharmacology of
Purinergic Transmission, University of Milan, via Balzaretti 9, 20133 Milan, Italy.
(Burnstock) Autonomic Neuroscience Centre, Royal Free and University College Medical School, Rowland Hill
Street, London, NW3 2PF, United Kingdom.
(Verkhratsky) Faculty of Life Sciences, The University of Manchester, Oxford Road, Manchester, M13 9PT, United
Kingdom.
(Verkhratsky) Institute of Experimental Medicine, ASCR, Videnska 1083, 14220 Prague, Czech Republic.
(Zimmermann) Goethe-University, Biocenter, Institute of Cell Biology and Neuroscience, Marie-Curie-Strasse 9, D60439 Frankfurt am Main, Germany.
Country of Publication
United Kingdom
Title
Purinergic signalling in the nervous system: an overview.
Source
Trends in Neurosciences. 32(1)(pp 19-29), 2009. Date of Publication: January 2009.
Publisher
Elsevier Ltd
Abstract
Purinergic receptors, represented by several families, are arguably the most abundant
receptors in living organisms and appeared early in evolution. After slow acceptance,
purinergic signalling in both peripheral and central nervous systems is a rapidly expanding
field. Here, we emphasize purinergic co-transmission, mechanisms of release and breakdown
of ATP, ion channel and G-protein-coupled-receptor subtypes for purines and pyrimidines, the
role of purines and pyrimidines in neuron-glial communication and interactions of this system
with other transmitter systems. We also highlight recent data involving purinergic signalling in
pathological conditions, including pain, trauma, ischaemia, epilepsy, migraine, psychiatric
disorders and drug addiction, which we expect will lead to the development of therapeutic
strategies for these disorders with novel mechanisms of action. copyright 2008 Elsevier Ltd.
All rights reserved.
ISSN 0166-2236
Publication Type Journal: Review
Journal Name Trends in Neurosciences
Volume 32
Issue Part 1
Page 19-29
Year of Publication 2009
Date of Publication January 2009
NEURO 2009 <233>
Database EMBASE
Accession Number 2009026731
Authors Naqvi N.H. Bechara A.
Institution
(Naqvi) Department of Psychiatry, Columbia University, New York State Psychiatric Institute, New York, NY 1032,
United States.
(Bechara) Brain and Creativity Institute, Department of Psychology, University of Southern California, Los Angeles,
CA 90089-2520, United States.
Country of Publication
United Kingdom
Title
The hidden island of addiction: the insula.
Source
Trends in Neurosciences. 32(1)(pp 56-67), 2009. Date of Publication: January 2009.
Publisher
Elsevier Ltd
Abstract
Most prior research on the neurobiology of addiction has focused on the role of subcortical
systems, such as the amygdala, the ventral striatum and mesolimbic dopamine system, in
promoting the motivation to seek drugs. Recent evidence indicates that a largely overlooked
structure, the insula, plays a crucial part in conscious urges to take drugs. The insula has
been highlighted as a region that integrates interoceptive (i.e. bodily) states into conscious
feelings and into decision-making processes that involve uncertain risk and reward. Here, we
propose a model in which the processing of the interoceptive effects of drug use by the insula
contributes to conscious drug urges and to decision-making processes that precipitate
relapse. copyright 2008 Elsevier Ltd. All rights reserved.
ISSN 0166-2236
Publication Type Journal: Review
Journal Name Trends in Neurosciences
Volume 32
Issue Part 1
Page 56-67
Year of Publication 2009
Date of Publication January 2009
NEURO 2009 <316>
Database EMBASE
Accession Number 2009302972
Authors Xiao C. Yang K.-C. Zhou C.-Y. Jin G.-Z. Wu J. Ye J.-H.
Institution
(Xiao, Zhou, Ye) Department of Anesthesiology, Pharmacology and Physiology, New Jersey Medical School,
UMDNJ, Newark, NJ 07103, United States.
(Yang, Wu) Divisions of Neurology, Barrow Neurological Institute, St Josephgs Hospital and Medical Center,
Phoenix, AZ 85013, United States.
(Yang, Jin) Department of Pharmacology, Shanghai Institute of Materia Medica, Chinese Academy of Sciences,
Shanghai 201203, China.
Country of Publication
United Kingdom
Title
Nicotine modulates GABAergic transmission to dopaminergic neurons in substantia
nigra pars compacta.
Source
Acta Pharmacologica Sinica. 30(6)(pp 851-858), 2009. Date of Publication: June 2009.
Publisher
Nature Publishing Group
Abstract
Aim: Dopaminergic neurons in the substantia nigra pars compacta (SNc) play important
roles in motor control and drug addiction. As the major afferent, GABAergic innervation
controls the activity of SNc dopaminergic neurons. Although it is clear that nicotine modulates
SNc dopaminergic neurons by activating subtypes of somatodendritic nicotinic acetylcholine
receptors (nAChRs), the detailed mechanisms of this activation remain to be addressed.
Methods: In the current study, we recorded GABA A receptor-mediated spontaneous
inhibitory postsynaptic currents (sIPSCs) from dissociated SNc dopaminergic neurons that
were obtained using an enzyme-free procedure. These neurons preserved some functional
terminals after isolation, including those that release GABA. Results: We found that both
extra- and intra-cellular calcium modulates sIPSCs in these neurons. Furthermore, both
nicotine and endogenous acetylcholine enhance the frequency of sIPSCs. Moreover,
endogenous acetylcholine tonically facilitates sIPSC frequency, primarily by activating the
alpha4B2 nAChRs on the GABAergic terminals. Conclusion: Nicotine facilitates GABA
release onto SNc dopaminergic neurons mainly via the activation of presynaptic alpha4B2
nAChRs. copyright 2009 CPS and SIMM.
ISSN 1671-4083
Publication Type Journal: Article
Journal Name Acta Pharmacologica Sinica
Volume 30
Issue Part 6
Page 851-858
Year of Publication 2009
Date of Publication June 2009
NEURO (A) 2009 <317>
Database EMBASE
Accession Number 2009302970
Authors Yang K.-C. Jin G.-Z. Wu J.
Institution
(Yang, Wu) Divisions of Neurology, Barrow Neurological Institute, St Joseph's Hospital and Medical Center,
Phoenix, AZ 85013, United States.
(Yang, Jin) Department of Pharmacology, Shanghai Institute of Materia Medica, Chinese Academy of Sciences,
Shanghai 201203, China.
Country of Publication
United Kingdom
Title
Mysterious
alpha6-containing
nAChRs:
Function,
pharmacology,
and
pathophysiology.
Source
Acta Pharmacologica Sinica. 30(6)(pp 740-751), 2009. Date of Publication: June 2009.
Publisher
Nature Publishing Group
Abstract
Neuronal nicotinic acetylcholine receptors (nAChRs) are the superfamily of ligand-gated ion
channels and widely expressed throughout the central and peripheral nervous systems.
nAChRs play crucial roles in modulating a wide range of higher cognitive functions by
mediating presynaptic, postsynaptic, and extrasynaptic signaling. Thus far, nine alpha
(alpha2-alpha10) and three beta (B2, B3, and B4) subunits have been identified in the CNS,
and these subunits assemble to form a diversity of functional nAChRs. Although alpha4B2and alpha7-nAChRs are the two major functional nAChR types in the CNS, alpha6-nAChRs
are abundantly expressed in the midbrain dopaminergic (DAergic) system, including
mesocorticolimbic and nigrostriatal pathways, and particularly present in presynaptic nerve
terminals. Recently, functional and pharmacological profiles of alpha6-nAChRs have been
assessed with the use of alpha6 subunit blockers such as alpha-conotoxin MII and PIA, and
also by using alpha6 subunit knockout mice. By modulating DA release in the nucleus
accumbens (NAc) and modulating GABA release onto DAergic neurons in the ventral
tegmental area (VTA), alpha6-nAChRs may play important roles in the mediation of nicotine
reward and addiction. Furthermore, alpha6-nAChRs in the nigrostriatal DAergic system may
be promising targets for selective preventative treatment of Parkinson's disease (PD). Thus,
alpha6-nAChRs may hold promise for future clinical treatment of human disorders, such as
nicotine addiction and PD. In this review, we mainly focus on the recent advances in the
understanding of alpha6-nAChR function, pharmacology and pathophysiology. copyright 2009
CPS and SIMM.
ISSN 1671-4083
Publication Type Journal: Review
Journal Name Acta Pharmacologica Sinica
Volume 30
Issue Part 6
Page 740-751
Year of Publication 2009
Date of Publication June 2009
NEURO 2009 <319>
Database EMBASE
Accession Number 2009302962
Authors Placzek A.N. Zhang T.A. Dani J.A.
Institution
(Placzek, Zhang, Dani) Department of Neuroscience, Baylor College of Medicine, Houston, TX 77030, United
States.
(Dani) Menninger Department of Psychiatry and Behavioral Sciences, Baylor College of Medicine, Houston, TX
77030, United States.
Country of Publication
United Kingdom
Title
Nicotinic mechanisms influencing synaptic plasticity in the hippocampus.
Source
Acta Pharmacologica Sinica. 30(6)(pp 752-760), 2009. Date of Publication: June 2009.
Publisher
Nature Publishing Group
Abstract
Nicotinic acetylcholine receptors (nAChRs) are expressed throughout the hippocampus, and
nicotinic signaling plays an important role in neuronal function. In the context of learning and
memory related behaviors associated with hippocampal function, a potentially significant
feature of nAChR activity is the impact it has on synaptic plasticity. Synaptic plasticity in
hippocampal neurons has long been considered a contributing cellular mechanism of learning
and memory. These same kinds of cellular mechanisms are a factor in the development of
nicotine addiction. Nicotinic signaling has been demonstrated by in vitro studies to affect
synaptic plasticity in hippocampal neurons via multiple steps, and the signaling has also been
shown to evoke synaptic plasticity in vivo. This review focuses on the nAChRs subtypes that
contribute to hippocampal synaptic plasticity at the cellular and circuit level. It also considers
nicotinic influences over long-term changes in the hippocampus that may contribute to
addiction. copyright 2009 CPS and SIMM.
ISSN 1671-4083
Publication Type Journal: Review
Journal Name Acta Pharmacologica Sinica
Volume 30
Issue Part 6
Page 752-760
Year of Publication 2009
Date of Publication June 2009
NEURO 2009 <321>
Database EMBASE
Accession Number 2009300590
Authors Indlekofer F. Piechatzek M. Daamen M. Glasmacher C. Lieb R. Pfister H. Tucha O. Lange K.W. Wittchen
H.U. Schutz C.G.
Institution
(Indlekofer, Piechatzek) Department of Psychiatry and Psychotherapy, Ludwig Maximilian University, Munich,
Germany.
(Daamen, Glasmacher, Schutz) Department of Psychiatry and Psychotherapy, Friedrich Wilhelm University, Bonn,
Germany.
(Lieb, Pfister, Wittchen) Max Planck Institute for Psychiatry, Munich, Germany.
(Tucha) School of Psychology, University of Plymouth, Plymouth, Devon, United Kingdom.
(Lange) Department of Experimental Psychology, University of Regensburg, Regensburg, Germany.
(Wittchen) Department of Psychiatry and Psychotherapy, University of Dresden, Dresden, Germany.
(Schutz) Institute of Mental Health, University of British Columbia, Vancouver, BC, Canada.
(Schutz) Institute of Mental Health, University of British Columbia, David Strangway Building, 5950 University
Boulevard, Vancouver, BC V6T 1Z3, Canada.
Country of Publication
United Kingdom
Title
Reduced memory and attention performance in a population-based sample of young
adults with a moderate lifetime use of cannabis, ecstasy and alcohol.
Source
Journal of Psychopharmacology. 23(5)(pp 495-509), 2009. Date of Publication: July 2009.
Publisher
SAGE Publications Ltd
Abstract
Regular use of illegal drugs is suspected to cause cognitive impairments. Two substances
have received heightened attention: 3,4- methylenedioxymethamphetamine (MDMA
orecstasy[trademark]) and ?-9-tetrahydrocannabinol (THC or cannabi). Preclinical evidence,
as well as human studies examining regular ecstasy consumers, indicated that ecstasy use
may have negative effects on learning, verbal memory and complex attentional functions.
Cannabis has also been linked to symptoms of inattention and deficits in learning and
memory. Most of the published studies in this field of research recruited participants by
means of newspaper advertisements or by using word-of-mouth strategies. Because
participants were usually aware that their drug use was critical to the research design, this
awareness may have caused selection bias or created expectation effects. Focussing on
attention and memory, this study aimed to assess cognitive functioning in a community-based
representative sample that was derived from a large-scale epidemiological study. Available
data concerning drug use history allowed sampling of subjects with varying degrees of lifetime
drug experiences. Cognitive functioning was examined in 284 young participants, between 22
and 34?years. In general, their lifetime drug experience was moderate. Participants
completed a neuropsychological test battery, including measures for verbal learning, memory
and various attentional functions. Linear regression analysis was performed to investigate the
relationship between cognitive functioning and lifetime experience of drug use. Ecstasy and
cannabis use were significantly related to poorer episodic memory function in a dose-related
manner. For attentional measures, decrements of small effect sizes were found. Error
measures in tonic and phasic alertness tasks, selective attention task and vigilance showed
small but significant effects, suggesting a stronger tendency to experience lapses of attention.
No indication for differences in reaction time was found. The results are consistent with
decrements of memory and attentional performance described in previous studies. These
effects are relatively small; however, it must be kept in mind that this study focussed on
assessing young adults with moderate drug use from a population-based study. copyright
2009 British Association for Psychopharmacology.
ISSN 0269-8811
Publication Type Journal: Article
Journal Name Journal of Psychopharmacology
Volume 23
Issue Part 5
Page 495-509
Year of Publication 2009
Date of Publication July 2009
NEURO (A) 2009 <322>
Database EMBASE
Accession Number 2009293206
Authors Wang Y. Ghezzi A. Yin J.C.P. Atkinson N.S.
Institution
(Wang, Ghezzi, Atkinson) Section of Neurobiology, University of Texas at Austin, Austin, TX,
(Wang, Atkinson) Waggoner Center for Alcohol and Addiction Research, University of Texas at Austin, Austin, TX,
(Yin) Department of Genetics, University of Wisconsin-Madison, Madison, WI,
(Yin) Department of Psychiatry, University of Wisconsin-Madison, Madison, WI, United States.
(Atkinson) Section of Neurobiology, University of Texas at Austin, 1 University Station C0920, Austin, TX 787120248, United States.
Country of Publication
United Kingdom
Title
CREB regulation of BK channel gene expression underlies rapid drug tolerance.
Source
Genes, Brain and Behavior. 8(4)(pp 369-376), 2009. Date of Publication: June 2009.
Publisher
Blackwell Publishing Ltd
Abstract
Pharmacodynamic tolerance is believed to involve homeostatic mechanisms initiated to
restore normal neural function. Drosophila exposed to a sedating dose of an organic solvent,
such as benzyl alcohol or ethanol, acquire tolerance to subsequent sedation by that solvent.
The slo gene encodes BK-type Ca 2+-activated K+ channels and has been linked to alcoholand organic solvent-induced behavioral tolerance in mice, Caenorhabditis elegans (C.
elegans) and Drosophila. The cyclic AMP response element-binding (CREB) proteins are
transcription factors that have been mechanistically linked to some behavioral changes
associated with drug addiction. Here, we show that benzyl alcohol sedation alters expression
of both dCREB-A and dCREB2-b genes to increase production of positively acting CREB
isoforms and to reduce expression of negatively acting CREB variants. Using a CREBresponsive reporter gene, we show that benzyl alcohol sedation increases CREB-mediated
transcription. Chromatin immunoprecipitation assays show that the binding of dCREB2, with a
phosphorylated kinase-inducible domain, increases immediately after benzyl alcohol sedation
within the slo promoter region. Most importantly, we show that a loss-of-function allele of
dCREB2 eliminates drug-induced upregulation of slo expression and the production of benzyl
alcohol tolerance. This unambiguously links dCREB2 transcription factors to these two benzyl
alcohol-induced phenotypes. These findings suggest that CREB positively regulates the
expression of slo-encoded BK-type Ca2+-activated K+ channels and that this gives rise to
behavioral tolerance to benzyl alcohol sedation. copyright 2009 Blackwell Publishing
Ltd/International Behavioural and Neural Genetics Society.
ISSN 1601-1848
Publication Type Journal: Article
Journal Name Genes, Brain and Behavior
Volume 8
Issue Part 4
Page 369-376
Year of Publication 2009
Date of Publication June 2009
NEURO 2009 <332>
Database EMBASE
Accession Number 2009320399
Authors Dagher A.
Institution
(Dagher) Department of Neurology, Montreal Neurological Institute, McGill University, 3801 University St., Montreal,
QC H3A 2B4, Canada.
Country of Publication
United Kingdom
Title
The neurobiology of appetite: Hunger as addiction.
Source
International Journal of Obesity. 33(SUPPL. 2)(pp S30-S33), 2009. Date of Publication:
June 2009.
Publisher
Nature Publishing Group
Abstract
Obesity is now being recognized as a neurobehavioral disorder. Although the view of
appetite as an addiction to food is controversial, there are useful lessons to be learned from
the neuroscience of addiction for understanding obesity. The speakers in this symposium all
addressed different aspects of the neurobiology of feeding and obesity. In this overview and
the associated reviews, the behavioral, genetic and neural factors that promote over-eating in
animals and humans are discussed. copyright 2009 Macmillan Publishers Limited.
ISSN 0307-0565
Publication Type Journal: Conference Paper
Journal Name International Journal of Obesity
Volume 33
Issue Part SUPPL. 2
Page S30-S33
Year of Publication 2009
Date of Publication June 2009
NEURO 2009 <333>
Database EMBASE
Accession Number 2009320398
Authors Dileone R.J.
Institution
(Dileone) Department of Molecular Psychiatry, Yale University School of Medicine, 34 Park St., New Haven, CT
06508, United States.
Country of Publication
United Kingdom
Title
The influence of leptin on the dopamine system and implications for ingestive
behavior.
Source
International Journal of Obesity. 33(SUPPL. 2)(pp S25-S29), 2009. Date of Publication:
June 2009.
Publisher
Nature Publishing Group
Abstract
Food intake is regulated by many factors, including sensory information, metabolic
hormones and the state of hunger. In modern humans, the drive to eat has proven to be
incompatible with the excess food supply present in industrialized societies. A result of this
imbalance is the dramatically increased rates of obesity during the last 20 years. The rise in
obesity rates poses one of the most significant public health issues facing the United States
and yet we do not understand the neural basis of ingestive behavior, and specifically, our
motivation to eat. Understanding how the brain controls eating will lay the foundation for
systematic dissection, understanding and treatment of obesity and related disorders. The lack
of control over food intake bears resemblance to drug addiction, where loss of control over
behavior leads to compulsive drug use. Work in laboratory animals has long suggested that
there exist common neural substrates underlying both food and drug intake behaviors. Recent
studies have shown direct leptin effects on dopamine neuron function and behavior. This
provides a new mechanism by which peripheral hormones influence behavior and contribute
to a more comprehensive model of neural control over food intake. copyright 2009 Macmillan
Publishers Limited.
ISSN 0307-0565
Publication Type Journal: Conference Paper
Journal Name International Journal of Obesity
Volume 33
Issue Part SUPPL. 2
Page S25-S29
Year of Publication 2009
Date of Publication June 2009
NEURO 2009 <348>
Database EMBASE
Accession Number 2009303411
Authors Dalley J.W. Everitt B.J.
Institution
(Dalley, Everitt) Behavioural and Clinical Neuroscience Institute, Department of Experimental Psychology, University
of Cambridge, Downing Street, Cambridge, CB2 3EB, United Kingdom.
(Dalley) Department of Psychiatry, University of Cambridge, Addenbrooke's Hospital, Cambridge, CB2 2QQ, United
Kingdom.
Country of Publication
United Kingdom
Title
Dopamine receptors in the learning, memory and drug reward circuitry.
Source
Seminars in Cell and Developmental Biology. 20(4)(pp 403-410), 2009. Date of Publication:
June 2009.
Publisher
Academic Press
Abstract
As primary targets of a variety of abused drugs G-protein-coupled dopamine receptors in the
brain play an important role in mediating the various drug-induced alterations in neural and
psychological processes thought to underlie the transition from voluntary drug use to habitual
and progressively compulsive drug-taking. This review considers the functional involvement of
the five major dopamine receptor subtypes in drug reinforcement and reward and discusses
the development of addiction as a series of learning transitions from initial goal-directed
behaviour to pathological stimulus-response habits in which drug-seeking behaviours are
automatically elicited and maintained by cues and stimuli associated with drug rewards.
copyright 2009 Elsevier Ltd. All rights reserved.
ISSN 1084-9521
Publication Type Journal: Review
Journal Name Seminars in Cell and Developmental Biology
Volume 20
Issue Part 4
Page 403-410
Year of Publication 2009
Date of Publication June 2009
NEURO 2009 <349>
Database EMBASE
Accession Number 2009303412
Authors Renthal W. Nestler E.J.
Institution
(Renthal) Departments of Psychiatry and Neuroscience, The University of Texas Southwestern Medical Center,
Dallas, TX, United States.
(Nestler) Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY, United States.
Country of Publication
United Kingdom
Title
Histone acetylation in drug addiction.
Source
Seminars in Cell and Developmental Biology. 20(4)(pp 387-394), 2009. Date of Publication:
June 2009.
Publisher
Academic Press
Abstract
Regulation of chromatin structure through post-translational modifications of histones (e.g.,
acetylation) has emerged as an important mechanism to translate a variety of environmental
stimuli, including drugs of abuse, into specific changes in gene expression. Since alterations
in gene expression are thought to contribute to the development and maintenance of the
addicted state, recent efforts are aimed at identifying how drugs of abuse alter chromatin
structure and the enzymes which regulate it. This review discusses how drugs of abuse alter
histone acetylation in brain reward regions, through which enzymes this occurs, and
ultimately what role histone acetylation plays in addiction-related behaviors. copyright 2009
Elsevier Ltd. All rights reserved.
ISSN 1084-9521
Publication Type Journal: Review
Journal Name Seminars in Cell and Developmental Biology
Volume 20
Issue Part 4
Page 387-394
Year of Publication 2009
Date of Publication June 2009
NEURO (A) 2009 <352>
Database EMBASE
Accession Number 2009272374
Authors Hipolito L. Sanchez-Catalan M.J. Granero L. Polache A.
Institution
(Hipolito, Sanchez-Catalan, Granero, Polache) Departamento de Farmacia y Tecnologia Farmaceutica, Universidad
de Valencia, Avda Vicente Andres Estelles s/n, 46100 Burjassot, Spain.
Country of Publication
United Kingdom
Title
Local salsolinol modulates dopamine extracellular levels from rat nucleus
accumbens: Shell/core differences.
Source
Neurochemistry International. 55(4)(pp 187-192), 2009. Date of Publication: September
2009.
Publisher
Elsevier Ltd
Abstract
Salsolinol (SAL), a condensation product of dopamine and acetaldehyde that appears in the
rat and human brain after ethanol ingestion, has been largely implicated in the aetiology of
alcoholism. Although the behavioural consequences of systemic or intracerebral SAL
administrations have been described, the neurochemical effects of pharmacologically relevant
doses of SAL and other tetrahydroisoquinolines (THIQs) in the brain areas involved in alcohol
addiction are practically unknown. To gain an insight into this topic, male Wistar rats were
stereotaxically implanted with one concentric microdialysis probe in either the shell or the core
of the nucleus accumbens (NAc). Treatments involved local administration of 0.1, 5 and 25
muM SAL for 20 min through the dialysis probe. Dopamine (DA) concentrations in the shell or
core of the NAc were on-line analyzed every 20 min by HPLC with electrochemical detection.
Implantation of the probe was histologically evaluated at the end of the experiments. Our
results indicate that dialysis application of 5 and 25 muM SAL into the core increased the
dialysate levels of DA. Conversely, the administration of the same doses of this drug into the
shell significantly reduced the DA levels in this subregion. In conclusion, these data reveal
that local application of SAL affects the DA levels in the NAc subterritories in a region-specific
manner. These findings may prove useful in probing CNS sites and mechanisms involved in
alcohol consumption. copyright 2009 Elsevier Ltd. All rights reserved.
ISSN 0197-0186
Publication Type Journal: Article
Journal Name Neurochemistry International
Volume 55
Issue Part 4
Page 187-192
Year of Publication 2009
Date of Publication September 2009
NEURO 2009 <367>
Database EMBASE
Accession Number 2009328922
Authors D'hoedt D. Bertrand D.
Institution
(D'hoedt, Bertrand) Department of Neurosciences, CMU, rue Michel-Servet 1, 1206 Geneve, Switzerland.
Country of Publication
United Kingdom
Title
Nicotinic acetylcholine receptors: An overview on drug discovery.
Source
Expert Opinion on Therapeutic Targets. 13(4)(pp 395-411), 2009. Date of Publication: April
2009.
Publisher
Informa Healthcare
Abstract
Background: Nicotinic acetylcholine receptors (nAChRs) are ligand-gated ion channels that
participate in many physiological functions. Receptors result from the assembly of five
homologous or heterologous subunits that form the ligand-binding site and an ionic pore. In
vertebrates, 17 subunits have been identified, beta(1-10), beta(1-4), gamma, delta and
epsilon. Assembly of different subunit combinations allows a diversity of physiological and
pharmacological properties. Objective: To review the putative involvement of nAChRs in
several diseases. Methods: We discuss the expression pattern of the subunits, the
pharmacological tools for distinguishing them and their role in pathogenesis.
Results/conclusion: Long-standing efforts in this field should soon result in the finding of new
molecules that might be applicable to situations ranging from neurological diseases to
immune treatments. copyright 2009 Informa UK Ltd. All rights reserved.
ISSN 1472-8222
Publication Type Journal: Review
Journal Name Expert Opinion on Therapeutic Targets
Volume 13
Issue Part 4
Page 395-411
Year of Publication 2009
Date of Publication April 2009
NEURO 2009 <369>
Database EMBASE
Accession Number 2009274240
Authors Zhang H. Li S. Wang M. Vukusic B. Pristupa Z.B. Liu F.
Institution
(Zhang, Li, Wang, Vukusic, Pristupa, Liu) Department of Neuroscience, Centre for Addiction and Mental Health,
Toronto, ON, Canada.
(Liu) Departments of Psychiatry, University of Toronto, Toronto, ON M5T 1R8, Canada.
Country of Publication
United Kingdom
Title
Regulation of dopamine transporter activity by carboxypeptidase e.
Source
Molecular Brain. 2(1), 2009. Article Number: 10. Date of Publication: 2009.
Publisher
BioMed Central Ltd.
Abstract
Background. The dopamine transporter (DAT) plays a critical role in terminating the action of
dopamine by rapid reuptake into the presynaptic neuron. Previous studies have revealed that
the DAT carboxyl terminus (DAT-CT) can directly interact with other cellular proteins and
regulate DAT function and trafficking. Results. Here, we have identified that carboxypeptidase
E (CPE), a prohormone processing exopeptidase and sorting receptor for the regulated
secretory pathway, interacts with the DAT-CT and affects DAT function. Mammalian cell lines
coexpressing CPE and DAT exhibited increased DAT-mediated dopamine uptake activity
compared to cells expressing DAT alone. Moreover, coexpression of an interfering DAT-CT
minigene inhibited the effects of CPE on DAT. Functional changes caused by CPE could be
attributed to enhanced DAT expression and subsequent increase in DAT cell surface
localization, due to decreased DAT degradation. In addition, CPE association could reduce
the phosphorylation state of DAT on serine residues, potentially leading to reduced
internalization, thus stabilizing plasmalemmal DAT localization. Conclusion. Taken together,
our results reveal a novel role for CPE in the regulation of DAT trafficking and DAT-mediated
DA uptake, which may provide a novel target in the treatment of dopamine-governed
diseases such as drug addiction and obesity.
Publication Type Journal: Article
Journal Name Molecular Brain
Volume 2
Issue Part 1
Year of Publication 2009
Date of Publication 2009
NEURO (A) 2009 <371>
Database EMBASE
Accession Number 2009318831
Authors Blanchard M.M. Mendelsohn D. Stamp J.A.
Institution
(Blanchard, Mendelsohn, Stamp) Department of Psychology, Dalhousie University, 1355 Oxford St, Halifax, B3H
4J1, Canada.
Country of Publication
United Kingdom
Title
The HR/LR model: Further evidence as an animal model of sensation seeking.
Source
Neuroscience and Biobehavioral Reviews. 33(7)(pp 1145-1154), 2009. Date of Publication:
July 2009.
Publisher
Elsevier Ltd
Abstract
Sensation seeking is a personality trait characterized by risk-taking and the desire to
experience novel stimuli. Evidence suggests that sensation seeking may increase an
individual's psychological and neurobiological vulnerabilities to drug abuse. One potential
animal model of human sensation seeking is high response to novelty in rats. High
responders (HRs) prefer a novel environment to a familiar one and show an increase in
locomotor activity in the new environment. These rats also show lower levels of anxiety-like
behaviour on several tests. Furthermore, HRs display a much higher propensity to selfadminister psychostimulants compared to low responders (LRs). HR rats and sensation
seeking humans share a number of similarities, for instance both exhibit elevated mesolimbic
dopamine activity, which has been implicated in central reward signaling and drug addiction.
Evidence of common behavioural tendencies, physiological responses and gene expression
patterns suggest that the HR model could be used as an animal model to investigate
substance abuse in sensation seeking humans. copyright 2009 Elsevier Ltd. All rights
reserved.
ISSN 0149-7634
Publication Type Journal: Review
Journal Name Neuroscience and Biobehavioral Reviews
Volume 33
Issue Part 7
Page 1145-1154
Year of Publication 2009
Date of Publication July 2009
NEURO 2009 <389>
Database EMBASE
Accession Number 2009349830
Authors Singh S.M. Basu D.
Institution
(Singh, Basu) Department of Psychiatry, Postgraduate Institute of Medical Education and Research (PGIMER),
Chandigarh, India.
(Basu) Department of Psychiatry, PGIMER, Chandigarh 160012, India.
Country of Publication
United Kingdom
Title
The P300 event-related potential and its possible role as an endophenotype for
studying substance use disorders: A review.
Source
Addiction Biology. 14(3)(pp 298-309), 2009. Date of Publication: July 2009.
Publisher
Blackwell Publishing Ltd
Abstract
The concept of endophenotypes has gained popularity in recent years. This is because of
the potential that endophenotypes provide of measuring objective trait markers that are
simpler to access and assess than complex behavioral disease phenotypes themselves. The
simplicity, ease of measurement and the putative links to the etiology of the disease in the
study of an endophenotype has the potential promise of unraveling the genetic basis of the
disease in question. Of the various proposed endophenotypes, the P300 component of the
event-related potential has been used in studies on alcoholism, schizophrenia and
externalizing disorders. The current state of knowledge regarding the concept of
endophenotypes, P300 and the validity of P300 as an endophenotype with special reference
to substance use disorders is discussed in this review. The implications of the above are
discussed. copyright 2008 Society for the Study of Addiction.
ISSN 1355-6215
Publication Type Journal: Review
Journal Name Addiction Biology
Volume 14
Issue Part 3
Page 298-309
Year of Publication 2009
Date of Publication July 2009
NEURO 2009 <391>
Database EMBASE
Accession Number 2009348034
Authors D'Ascenzo M. Podda M.V. Fellin T. Azzena G.B. Haydon P. Grassi C.
Institution
(D'Ascenzo, Podda, Azzena, Grassi) Institute of Human Physiology, Medical School, Catholic University 'S. Cuore',
Largo Francesco Vito 1, 00168 Rome, Italy.
(Fellin) Italian Institute of Technology, Genoa, Italy.
(Haydon) Department of Neuroscience, Tufts University, Boston, MA, United States.
Country of Publication
United Kingdom
Title
Activation of mGluR5 induces spike afterdepolarization and enhanced excitability in
medium spiny neurons of the nucleus accumbens by modulating persistent Na+
currents.
Source
Journal of Physiology. 587(13)(pp 3233-3250), 2009. Date of Publication: 2009.
Publisher
Blackwell Publishing Ltd
Abstract
The involvement of metabotropic glutamate receptors type 5 (mGluR5) in drug-induced
behaviours is well-established but limited information is available on their functional roles in
addiction-relevant brain areas like the nucleus accumbens (NAc). This study demonstrates
that pharmacological and synaptic activation of mGluR5 increases the spike discharge of
medium spiny neurons (MSNs) in the NAc. This effect was associated with the appearance of
a slow afterdepolarization (ADP) which, in voltage-clamp experiments, was recorded as a
slowly inactivating inward current. Pharmacological studies showed that ADP was elicited by
mGluR5 stimulation via G-protein-dependent activation of phospholipase C and elevation of
intracellular Ca2+ levels. Both ADP and spike aftercurrents were significantly inhibited by the
Na+ channel-blocker, tetrodotoxin (TTX). Moreover, the selective blockade of persistent Na+
currents (INaP), achieved by NAc slice pre-incubation with 20 nM TTX or 10 muM riluzole,
significantly reduced the ADP amplitude, indicating that this type of Na+ current is responsible
for the mGluR5-dependent ADP. mGluR5 activation also produced significant increases in
INaP, and the pharmacological blockade of this current prevented the mGluR5-induced
enhancement of spike discharge. Collectively, these data suggest that mGluR5 activation
upregulates INaP in MSNs of the NAc, thereby inducing an ADP that results in enhanced
MSN excitability. Activation of mGluR5 will significantly alter spike firing in MSNs in vivo, and
this effect could be an important mechanism by which these receptors mediate certain
aspects of drug-induced behaviours. copyright 2009 The Author. Journal compilation
copyright 2009 The Physiological Society.
ISSN 0022-3751
Publication Type Journal: Article
Journal Name Journal of Physiology
Volume 587
Issue Part 13
Page 3233-3250
Year of Publication 2009
Date of Publication 2009
NEURO 2009 <392>
Database EMBASE
Accession Number 2009335423
Authors Antonini A. Tolosa E.
Institution
(Antonini) Parkinson Institute Milan, Istituti Clinici di Perfezionamento, Via Bignami 1, Milan, Italy.
(Tolosa) Parkinson's Disease and Movement Disorders Unit, Centro de Investigacion Biomedica en Red Sobre
Enfermedades Neurodegenerativas (CIBERNED), Hospital Clinic Universitari, Barcelona, Spain.
Country of Publication
United Kingdom
Title
Apomorphine and levodopa infusion therapies for advanced Parkinson's disease:
Selection criteria and patient management.
Source
Expert Review of Neurotherapeutics. 9(6)(pp 859-867), 2009. Date of Publication: June
2009.
Publisher
Expert Reviews Ltd.
Abstract
The continuous infusion of levodopa or apomorphine represents a good therapeutic option
for advanced Parkinson's disease as this approach provides constant dopaminergic
stimulations and is a good alternative to deep brain stimulation. While apomorphine provides
a similar level of motor benefit to levodopa, its long-term use is limited by compliance and
injection site skin reactions. The administration of levodopa/carbidopa by continuous
duodenal infusion allows replacement of all oral medications and permits achievement of a
satisfactory therapeutic response paralleled by a reduction in motor complication severity.
However, compared with apomorphine, it is more invasive as it requires a percutaneous
endoscopic gastrostomy. In this review we discuss the advantages and limitations of these
procedures and how they compare to deep brain stimulation. We also address the issue of
selection criteria and propose clinical characteristics of candidates to help the clinician choose
the most suitable option for their patients. copyright 2009 Expert Reviews Ltd.
ISSN 1473-7175
Publication Type Journal: Review
Journal Name Expert Review of Neurotherapeutics
Volume 9
Issue Part 6
Page 859-867
Year of Publication 2009
Date of Publication June 2009
NEURO 2009 <398>
Database EMBASE
Accession Number 2009372392
Authors Beardsley P.M. Thomas B.F. Mcmahon L.R.
Institution
(Beardsley) Department of Pharmacology and Toxicology, Virginia Commonwealth University, PO Box 980613,
Richmond, VA 23298-0613, United States.
(Thomas) Center for Chemistry Services, Health Sciences Unit, RTI International, Research Triangle Park, NC,
United States.
(Mcmahon) University of Texas Health Science Center, San Antonio, TX, United States.
Country of Publication
United Kingdom
Title
Cannabinoid CB1 receptor antagonists as potential pharmacotherapies for drug
abuse disorders.
Source
International Review of Psychiatry. 21(2 SPEC. ISS.)(pp 134-142), 2009. Date of
Publication: April 2009.
Publisher
Informa Healthcare
Abstract
Since the discovery of the cannabinoid CB1 receptor (CB1R) in 1988, and subsequently of
the CB2 receptor (CB2R) in 1993, there has been an exponential growth of research
investigating the functions of the endocannabinoid system. The roles of CB1Rs have been of
particular interest to psychiatry because of their selective presence within the CNS and
because of their association with brain-reward circuits involving mesocorticolimbic dopamine
systems. One potential role that has become of considerable focus is the ability of CB1Rs to
modulate the effects of the drugs of abuse. Many drugs of abuse elevate dopamine levels,
and the ability of CB1R antagonists or inverse agonists to modulate these elevations has
suggested their potential application as pharmacotherapies for treating drug abuse disorders.
With the identification of the selective CB1R antagonist, rimonabant, in 1994, and
subsequently of other CB1R antagonists, there has been a rapid expansion of research
investigating their ability to modulate the effects of the drugs of abuse. This review highlights
some of the preclinical and clinical studies that have examined the effects of CB1R
antagonists under conditions potentially predictive of their therapeutic efficacy as treatments
for drug abuse disorders. copyright 2009 Informa Healthcare USA, Inc.
ISSN 0954-0261
Publication Type Journal: Review
Journal Name International Review of Psychiatry
Volume 21
Issue Part 2 SPEC. ISS.
Page 134-142
Year of Publication 2009
Date of Publication April 2009
NEURO (A) 2009 <419>
Database EMBASE
Accession Number 2009363519
Authors Guo S.
Institution
(Guo) University of California San Francisco, Institute for Regenerative Medicine, Department of Biopharmaceutical
Sciences, CA 94143-2811, United States.
Country of Publication
United Kingdom
Title
Using zebrafish to assess the impact of drugs on neural development and function.
Source
Expert Opinion on Drug Discovery. 4(7)(pp 715-726), 2009. Date of Publication: July 2009.
Publisher
Informa Healthcare
Abstract
Background: Zebrafish is becoming an increasingly attractive model organism for
understanding biology and developing therapeutics, because as a vertebrate, it shares
considerable similarity with mammals in both genetic compositions and tissue/organ
structures, and yet remains accessible to high throughput phenotype-based genetic and small
molecule compound screening. Objective/method: The focus of this review is on the nervous
system, which is arguably the most complex organ and known to be afflicted by > 600
disorders in humans. I discuss the past, present and future of using zebrafish to assess the
impact of small molecule drugs on neural development and function, in light of understanding
and treating neurodevelopmental disorders such as autism, neurodegenerative disorders
including Alzheimer's, Parkinson's and Huntington's disease and neural system dysfunctions
such as anxiety/depression and addiction. Conclusion: These studies hold promise to reveal
fundamental mechanisms governing nervous system development and function, and to
facilitate small molecule drug discovery for the many types of neurological disorders.
copyright 2009 Informa UK Ltd. All rights reserved.
ISSN 1746-0441
Publication Type Journal: Review
Journal Name Expert Opinion on Drug Discovery
Volume 4
Issue Part 7
Page 715-726
Year of Publication 2009
Date of Publication July 2009
NEURO 2009 <437>
Database EMBASE
Accession Number 2009412451
Authors Latvala A. Castaneda A.E. Perala J. Saarni S.I. Aalto-Setala T. Lonnqvist J. Kaprio J. Suvisaari J. TuulioHenriksson A.
Institution
(Latvala, Castaneda, Perala, Saarni, Aalto-Setala, Lonnqvist, Kaprio, Suvisaari, Tuulio-Henriksson) Department of
Mental Health, Substance Abuse Services, National Institute for Health and Welfare, Mannerheimintie 166, FIN00271 Helsinki, Finland.
(Latvala, Castaneda, Tuulio-Henriksson) Department of Psychology, University of Helsinki, Finland.
(Aalto-Setala) Department of Child Psychiatry, Hospital for Children and Adolescents, Helsinki University Central
Hospital, Finland.
(Lonnqvist) Department of Psychiatry, University of Helsinki, Finland.
(Kaprio) Department of Public Health, University of Helsinki, Finland.
(Suvisaari) Department of Social Psychiatry, Tampere School of Public Health, University of Tampere, Finland.
Country of Publication
United Kingdom
Title
Cognitive functioning in substance abuse and dependence: A population-based study
of young adults.
Source
Addiction. 104(9)(pp 1558-1568), 2009. Date of Publication: September 2009.
Publisher
Blackwell Publishing Ltd
Abstract
Aims To investigate whether substance use disorders (SUDs) are associated with verbal
intellectual ability, psychomotor processing speed, verbal and visual working memory,
executive function and verbal learning in young adults, and to study the associations of SUD
characteristics with cognitive performance. Participants A population-based sample (n = 466)
of young Finnish adults aged 21-35 years. Measurements Diagnostic assessment was based
on all available information from a structured psychiatric interview (SCID-I) and in- and outpatient medical records. Established neuropsychological tests were used in the cognitive
assessment. Confounding factors included in the analyses were comorbid psychiatric
disorders and risk factors for SUDs, representing behavioural and affective factors, parental
factors, early initiation of substance use and education-related factors. Findings Adjusted for
age and gender, life-time DSM-IV SUD was associated with poorer verbal intellectual ability,
as measured with the Wechsler Adult Intelligence Scale-Revised (WAIS-R) vocabulary
subtest, and slower psychomotor processing, as measured with the WAIS-R digit symbol
subtest. Poorer verbal intellectual ability was accounted for by parental and own low basic
education, whereas the association with slower psychomotor processing remained after
adjustment for SUD risk factors. Poorer verbal intellectual ability was related to substance
abuse rather than dependence. Other SUD characteristics were not associated with cognition.
Conclusions Poorer verbal intellectual ability and less efficient psychomotor processing are
associated with life-time alcohol and other substance use disorders in young adulthood.
Poorer verbal intellectual ability seems to be related to parental and own low basic education,
whereas slower psychomotor processing is associated with SUD independently of risk
factors. copyright 2009 Society for the Study of Addiction.
ISSN 0965-2140
Publication Type Journal: Article
Journal Name Addiction
Volume 104
Issue Part 9
Page 1558-1568
Year of Publication 2009
Date of Publication September 2009