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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