NEURO 2009<452>
Database EMBASE
Accession Number 2009384631
Authors Niehaus J.L. Cruz-BermudezN.D. Kauer J.A.
Institution
(Niehaus, Cruz-Bermudez, Kauer) Department of Molecular Pharmacology, Physiology and Biotechnology, BrownUniversity, Providence, RI,
(Kauer) Department of Neuroscience, BrownUniversity, Providence, RI,
(Cruz-Bermudez) Universidad de Puerto Rico, Rio Piedras,
(Kauer) BrownUniversity, Box G-B4, Providence, RI02912,
Country of Publication
United Kingdom
Title
Plasticity of addiction: A mesolimbic dopamine short-circuit?
Source
American Journal on Addictions. 18(4)(pp 259-271), 2009. Date of Publication: July 2009.
Publisher
Informa Healthcare
Abstract
The development of drug addiction progresses along a continuum from acute drug use to compulsive use and drug seeking behavior. Many researchers have focused on identifying the physiological mechanisms involved in drug addiction in order to develop effective pharmacotherapies. Neuroplasticity, the putative mechanism underlying learning and memory, is modified by drugs of abuse and may contribute to the development of the eventual addicted state. Innovative treatments directly targeting these drug-induced changes in brain reward components and circuits may be efficacious in reducing drug use and relapse.
ISSN 1055-0496
Publication Type Journal: Review
Journal Name American Journal on Addictions
Volume 18
Issue Part 4
Page 259-271
Year of Publication 2009
Date of Publication July 2009
NEURO 2009<456>
Database EMBASE
Accession Number 2009384627
Authors Mysels D.
Institution
(Mysels) Columbia Presbyterian Medical Center, New York State Psychiatric Institution, Division on Substance Use Research, 1051 Riverside Drive, New York, NY 10032,
Country of Publication
United Kingdom
Title
The kappa-opiate receptor impacts the pathophysiology and behavior of substance use.
Source
American Journal on Addictions. 18(4)(pp 272-276), 2009. Date of Publication: July 2009.
Publisher
Informa Healthcare
Abstract
There is increasing evidence that the kappa-opiate receptor, in addition to the mu-opiate receptor, plays an important role in substance use pathophysiology and behavior. As dopamine activity is upregulated through chronic substance use, kappa receptor activity, mediated through the peptide dynorphin, is upregulated in parallel. Dynorphin causes dysphoria and decreased locomotion, and the upregulation of its activity on the kappa receptor likely dampens the excitation caused by increased dopaminergic activity. This feedback mechanism may have significant clinical implications for treating drug dependent patients in various stages of their pathology.
ISSN 1055-0496
Publication Type Journal: Article
Journal Name American Journal on Addictions
Volume 18
Issue Part 4
Page 272-276
Year of Publication 2009
Date of Publication July 2009
NEURO 2009<476>
Database EMBASE
Accession Number 2009401701
Authors Lee J.L.C.
Institution
(Lee) School of Psychology, University of Birmingham, Edgbaston, Birmingham, B15 2TT, United Kingdom.
Country of Publication
United Kingdom
Title
Reconsolidation: maintaining memory relevance.
Source
Trends in Neurosciences. 32(8)(pp 413-420), 2009. Date of Publication: August 2009.
Publisher
Elsevier Ltd
Abstract
The retrieval of a memory places it into a plastic state, the result of which is that the memory can be disrupted or even enhanced by experimental treatment. This phenomenon has been conceptualised within a framework of memories being reactivated and then reconsolidated in repeated rounds of cellular processing. The reconsolidation phase has been seized upon as crucial for the understanding of memory stability and, more recently, as a potential therapeutic target in the treatment of disorders such as post-traumatic stress and drug addiction. However, little is known about the reactivation process, or what might be the adaptive function of retrieval-induced plasticity. Reconsolidation has long been proposed to mediate memory updating, but only recently has this hypothesis been supported experimentally. Here, the adaptive function of memory reconsolidation is explored in more detail, with a strong emphasis on its role in updating memories to maintain their relevance. copyright 2009 Elsevier Ltd. All rights reserved.
ISSN 0166-2236
Publication Type Journal: Article
Journal Name Trends in Neurosciences
Volume 32
Issue Part 8
Page 413-420
Year of Publication 2009
Date of Publication August 2009
NEURO (A) 2009<485>
Database EMBASE
Accession Number 2009412426
Authors Wilson D.I.G. MacLaren D.A.A. Winn P.
Institution
(Wilson, MacLaren, Winn) School of Psychology, University of St Andrews, St Mary's Quad, South Street, St Andrews, Fife KY16 9JP, United Kingdom.
Country of Publication
United Kingdom
Title
Bar pressing for food: Differential consequences of lesions to the anterior versus posterior pedunculopontine.
Source
European Journal of Neuroscience. 30(3)(pp 504-513), 2009. Date of Publication: August 2009.
Publisher
Blackwell Publishing Ltd
Abstract
The pedunculopontine tegmental nucleus (PPTg) is in a key position to participate in operant reinforcement via its connections with the corticostriatal architecture and the medial reticular formation. Indeed, previous work has demonstrated that rats bearing lesions of the whole PPTg are impaired when learning to make two bar presses for amphetamine reinforcement. Anterior and posterior portions of the PPTg make different anatomical connections, including preferential projections by the anterior PPTg to substantia nigra pars compacta dopamine neurons and by the posterior PPTg to ventral tegmental area dopamine neurons. We wanted to assess the effects of anterior and posterior PPTg ibotenate lesions on rats learning simple and more complex schedules of natural reinforcement. We trained rats with lesions to the anterior PPTg (n = 11) and the posterior PPTg (n = 5) [and appropriate controls (n = 15)] to bar press for food on a variety of fixed-ratio and variable-ratio reinforcement schedules and then during extinction. We found that posterior PPTg-lesioned rats bar pressed at lower rates, were slower to learn to bar press, and often had deficits characteristic of impaired learning and/or motivation. In contrast, anterior PPTg-lesioned rats learned to bar press for reinforcement at normal rates. However, they made errors of perseveration and anticipation throughout many schedules, and pressed at a higher rate than controls during extinction, deficits best characterized as reflecting disorganized response control. Together, these data suggest that the anterior PPTg and posterior PPTg (and their related circuits) contribute differently to reinforcement learning, incentive motivation, and response control, processes that are considered to malfunction in drug addiction. copyright Federation of European Neuroscience Societies and Blackwell Publishing Ltd.
ISSN 0953-816X
Publication Type Journal: Article
Journal Name European Journal of Neuroscience
Volume 30
Issue Part 3
Page 504-513
Year of Publication 2009
Date of Publication August 2009
NEURO 2009<488>
Database EMBASE
Accession Number 2009376748
Authors Kalivas P.W.
Institution
(Kalivas) Department of Neurosciences, Medical University of South Carolina, Ashley Avenue, BSB 410, Charleston, SC 29425, United States.
Country of Publication
United Kingdom
Title
The glutamate homeostasis hypothesis of addiction.
Source
Nature Reviews Neuroscience. 10(8)(pp 561-572), 2009. Date of Publication: August 2009.
Publisher
Nature Publishing Group
Abstract
Addiction is associated with neuroplasticity in the corticostriatal brain circuitry that is important for guiding adaptive behaviour. The hierarchy of corticostriatal information processing that normally permits the prefrontal cortex to regulate reinforcement-seeking behaviours is impaired by chronic drug use. A failure of the prefrontal cortex to control drug-seeking behaviours can be linked to an enduring imbalance between synaptic and non-synaptic glutamate, termed glutamate homeostasis. The imbalance in glutamate homeostasis engenders changes in neuroplasticity that impair communication between the prefrontal cortex and the nucleus accumbens. Some of these pathological changes are amenable to new glutamate- and neuroplasticity-based pharmacotherapies for treating addiction. copyright 2009 Macmillan Publishers Limited. All rights reserved.
ISSN 1471-003X
Publication Type Journal: Review
Journal Name Nature Reviews Neuroscience
Volume 10
Issue Part 8
Page 561-572
Year of Publication 2009
Date of Publication August 2009
NEURO (A) 2009<496>
Database EMBASE
Accession Number 2009389909
Authors Sorensen G. Wegener G. Hasselstrom J. Hansen T.V.O. Wortwein G. Fink-Jensen A. Woldbye D.P.D.
Institution
(Sorensen, Wortwein, Fink-Jensen, Woldbye) Laboratory of Neuropsychiatry, Copenhagen Mental HealthCenter Rigshospitalet, Copenhagen, Denmark.
(Sorensen, Wortwein, Fink-Jensen, Woldbye) Department of Neuroscience and Pharmacology, University of Copenhagen, 9 Blegdamsvej, Copenhagen DK-2100, Denmark.
(Wegener, Hasselstrom) Centre for Psychiatric Research, AarhusUniversityHospital, Risskov, Denmark.
(Hansen) Department of Clinical Biochemistry, CopenhagenUniversityHospital Rigshospitalet, Copenhagen, Denmark.
(Woldbye) Laboratory of Neuropsychiatry, RigshospitaletUniversityHospital, Copenhagen DK-2100, Denmark.
Country of Publication
United Kingdom
Title
Neuropeptide Y infusion into the shell region of the rat nucleus accumbens increases extracellular levels of dopamine.
Source
NeuroReport. 20(11)(pp 1023-1026), 2009. Date of Publication: 15 Jul 2009.
Publisher
Lippincott Williams and Wilkins
Abstract
Increases in extracellular dopamine in the shell region of the nucleus accumbens are centrally involved in mediating reinforcement of addictive drugs. Neuropeptide Y (NPY) and its receptors are present in the nucleus accumbens and have been implicated in addiction mechanisms. This study further explored the potential role of NPY in addiction mechanisms using microdialysis to measure extracellular dopamine in vivo after infusion of NPY directly into the accumbal shell region of adult rats. NPY was found to dose-dependently increase extracellular dopamine levels, indicating that NPY could play an important role in drug reinforcement by modulating accumbal dopamine levels. copyright 2009 Lippincott Williams & Wilkins, Inc.
ISSN 0959-4965
Publication Type Journal: Article
Journal Name NeuroReport
Volume 20
Issue Part 11
Page 1023-1026
Year of Publication 2009
Date of Publication 15 Jul 2009
NEURO 2009<499>
Database EMBASE
Accession Number 2009430248
Authors Gubellini P. Salin P. Kerkerian-Le Goff L. Baunez C.
Institution
(Gubellini, Salin, Kerkerian-Le Goff) Institut de Biologie du Developpement de Marseille-Luminy (IBDML), UMR6216 CNRS/Universite de la Mediterranee, Case 907, Parc Scientifique Luminy, 13288 Marseille Cedex 9, France.
(Baunez) Laboratoire de Neurobiologie de la Cognition (LNC), UMR6155 CNRS, Marseille, France.
Country of Publication
United Kingdom
Title
Deep brain stimulation in neurological diseases and experimental models: From molecule to complex behavior.
Source
Progress in Neurobiology. 89(1)(pp 79-123), 2009. Date of Publication: September 2009.
Publisher
Elsevier Ltd
Abstract
Deep brain stimulation (DBS) has proven to be capable of providing significant benefits for several neuropathologies. It is highly effective in reducing the motor symptoms of Parkinson's disease, essential tremor, and dystonia, and in alleviating chronic pain. Recently, also Tourette syndrome, obsessive-compulsive disorder and treatment-resistant depression have been treated by DBS with encouraging results. However, despite these clinical achievements, the precise action mechanisms of DBS still need to be fully characterized. For this reason, several animal models of DBS have been developed, bringing new insights on the effects of this treatment at molecular and cellular level, and providing new evidence on its physiological and behavioral consequences. In parallel, physiological and imaging studies in patients have contributed to better understanding DBS impact on the function of brain circuits. Here we review the clinical data and experimental work in vitro, ex vivo and in vivo (mostly arisen from studies on DBS of the subthalamic nucleus) in the treatment of PD, which led to the actual knowledge of DBS mechanisms, from molecular to complex behavioral levels. copyright 2009 Elsevier Ltd. All rights reserved.
ISSN 0301-0082
Publication Type Journal: Review
Journal Name Progress in Neurobiology
Volume 89
Issue Part 1
Page 79-123
Year of Publication 2009
Date of Publication September 2009
NEURO 2009<509>
Database EMBASE
Accession Number 2009452934
Authors Sun X. Wolf M.E.
Institution
(Sun, Wolf) Department of Neuroscience, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064, United States.
Country of Publication
United Kingdom
Title
Nucleus accumbens neurons exhibit synaptic scaling that is occluded by repeated dopamine pre-exposure.
Source
European Journal of Neuroscience. 30(4)(pp 539-550), 2009. Date of Publication: August 2009.
Publisher
Blackwell Publishing Ltd
Abstract
Synaptic scaling has been proposed as a form of plasticity that may contribute to drug addiction but it has not been previously demonstrated in the nucleus accumbens (NAc), a critical region for addiction. Here we demonstrate bidirectional synaptic scaling in postnatal rat NAc neurons that were co-cultured with prefrontal cortical neurons to restore excitatory input. Prolonged activity blockade (1-3 days) with an AMPA receptor antagonist increased cell surface (synaptic and extrasynaptic) glutamate receptor 1 (GluR1) and GluR2 but not GluR3, as well as GluR1/2 co-localization on the cell surface and total GluR1 and GluR2 protein levels. A prolonged increase in activity (bicuculline, 48 h) produced opposite effects. These results suggest that GluR1/2-containing AMPA receptors undergo synaptic scaling in NAc neurons. GluR1 and GluR2 surface expression was also increased by tetrodotoxin alone or in combination with an N-methyl-d-aspartate receptor or AMPA receptor antagonist but not by the l-type Ca2+ channel antagonist nifedipine. A cobalt-quenching assay confirmed the immunocytochemical results indicating that synaptic scaling after activity blockade did not involve a change in abundance of GluR2-lacking AMPA receptors. Increased AMPA receptor surface expression after activity blockade required protein synthesis and was occluded by inhibition of the ubiquitin-proteasome system. Repeated dopamine (DA) treatment, which leads to upregulation of surface GluR1 and GluR2, occluded activity blockade-induced synaptic scaling. These latter results indicate an interaction between cellular mechanisms involved in synaptic scaling and adaptive mechanisms triggered by repeated DA receptor stimulation, suggesting that synaptic scaling may not function normally after exposure to DA-releasing drugs such as cocaine. copyright 2009 Federation of European Neuroscience Societies and Blackwell Publishing Ltd.
ISSN 0953-816X
Publication Type Journal: Article
Journal Name European Journal of Neuroscience
Volume 30
Issue Part 4
Page 539-550
Year of Publication 2009
Date of Publication August 2009
NEURO 2009<522>
Database EMBASE
Accession Number 2009429236
Authors Uhl G.R. Drgon T. Johnson C. Liu Q.-R.
Institution
(Uhl, Drgon, Johnson, Liu) Molecular Neurobiology Branch, NIH-IRP (NIDA), Box 5180, Baltimore, MD21224, United States.
Country of Publication
United Kingdom
Title
Addiction genetics and pleiotropic effects of common haplotypes that make polygenic contributions to vulnerability to substance dependence.
Source
Journal of Neurogenetics. 23(3)(pp 272-282), 2009. Date of Publication: January 2009.
Publisher
Informa Healthcare
Abstract
Abundant evidence from family, adoption, and twin studies point to large genetic contributions to individual differences in vulnerability to develop dependence on one or more addictive substances. Twin data suggest that most of this genetic vulnerability is shared by individuals who are dependent on a variety of addictive substances. Molecular genetic studies, especially genomewide and candidate gene association studies, have elucidated common haplotypes in dozens of genes that appear to make polygenic contributions to vulnerability to developing dependence. Most genes that harbor currently identified addiction-associated haplotypes are expressed in the brain. Haplotypes in many of the same genes are identified in genomewide association studies that compare allele frequencies in substance dependent vs. control individuals from European, African, and Asian racial/ethnic backgrounds. Many of these addiction-associated haplotypes display pleiotropic influences on a variety of related brain-based phenotypes that display 1) substantial heritability and 2) clinical cooccurence with substance dependence. Copyright copyright 2009 Informa UK Ltd.
ISSN 0167-7063
Publication Type Journal: Review
Journal Name Journal of Neurogenetics
Volume 23
Issue Part 3
Page 272-282
Year of Publication 2009
Date of Publication January 2009
NEURO (A) 2009<540>
Database EMBASE
Accession Number 2009481208
Authors Cifani C. Zanoncelli A. Tessari M. Righetti C. Di Francesco C. Ciccocioppo R. Massi M. Melotto S.
Institution
(Cifani, Ciccocioppo, Massi) Department of Experimental Medicine and Public Health, University of Camerino, Via Madonna delle Carceri, 62032 Camerino, Italy.
(Zanoncelli, Tessari, Righetti, Di Francesco, Melotto) Department of Biology, Neurosciences CEDD, GlaxoSmithKline Medicines Research Centre, Via Fleming 4, 37135 Verona, Italy.
Country of Publication
United Kingdom
Title
Pre-exposure to environmental cues predictive of food availability elicits hypothalamic-pituitary-adrenal axis activation and increases operant responding for food in female rats.
Source
Addiction Biology. 14(4)(pp 397-407), 2009. Date of Publication: October 2009.
Publisher
Blackwell Publishing Ltd
Abstract
The present study was undertaken to develop an animal model exploiting food cue-induced increased motivation to obtain food under operant self-administration conditions. To demonstrate the predictive validity of the model, rimonabant, fluoxetine, sibutramine and topiramate, administered 1 hour before the experiment, were tested. For 5 days, female Wistar rats were trained to self-administer standard 45 mg food pellets in one daily session (30 minutes) under FR1 (fixed ratio 1) schedule of reinforcement. Rats were then trained to an FR3 schedule and finally divided into two groups. The first group (control) was subjected to a standard 30 minutes FR3 food self-administration session. The second group was exposed to five presentations of levers and light for 10 seconds each (every 3 minutes in 15 minutes total). At the completion of this pre-session phase, a normal 30-minute session (as in the control group) started. Results showed that pre-exposure to environmental stimuli associated to food deliveries increased response for food when the session started. Corticosterone and adrenocorticotropic hormone plasma levels, measured after the 15-minute pre-exposure, were also significantly increased. No changes were observed for the other measured hormones (growth hormone, prolactin, thyroid-stimulating hormone, luteinizing hormone, insulin, amylin, gastric inhibitor polypeptide, ghrelin, leptin, peptide YY and pancreatic polypeptide). Rimonabant, sibutramine and fluoxetine significantly reduced food intake in both animals pre-exposed and in those not pre-exposed to food-associated cues. Topiramate selectively reduced feeding only in pre-exposed rats. The present study describes the development of a new animal model to investigate cue-induced increased motivation to obtain food. This model shows face and predictive validity, thus, supporting its usefulness in the investigation of new potential treatments of binge-related eating disorders. In addition, the present findings confirm that topiramate may represent an important pharmacotherapeutic approach to binge-related eating. copyright 2009 Society for the Study of Addiction.
ISSN 1355-6215
Publication Type Journal: Article
Journal Name Addiction Biology
Volume 14
Issue Part 4
Page 397-407
Year of Publication 2009
Date of Publication October 2009
NEURO 2009<557>
Database EMBASE
Accession Number 2009430469
Authors Navarro H.A. Howard J.L. Pollard G.T. Carroll F.I.
Institution
(Navarro) Research Triangle Institute, Post Office Box 12194, Research Triangle Park, NC27709-2194, United States.