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  1. Book: Neuropsychopharmacology: A tribute to Joseph T. Coyle

    Coyle, Joseph T. / Schwarcz, Robert

    (Advances in pharmacology ; volume 76)

    2016  

    Author's details edited by Robert Schwarcz
    Series title Advances in pharmacology ; volume 76
    Collection
    Language English
    Size XX, 400 Seiten, Illustrationen
    Edition First edition
    Publisher Elsevier
    Publishing place Amsterdam
    Publishing country Netherlands
    Document type Book
    HBZ-ID HT019029097
    ISBN 978-0-12-809745-8 ; 0-12-809745-0
    Database Catalogue ZB MED Medicine, Health

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  2. Book: Neurobiology of brain disorders

    Zigmond, Michael J. / Rowland, Lewis P. / Coyle, Joseph T.

    biological basis of neurological and psychiatric disorders

    2015  

    Author's details ed. by Michael J. Zigmond ; Lewis P. Rowland ; Joseph T. Coyle
    Language English
    Size XIX, 801 S. : Ill., graph. Darst.
    Publisher Elsevier AP
    Publishing place Amsterdam u.a.
    Publishing country Netherlands
    Document type Book
    HBZ-ID HT018490941
    ISBN 978-0-12-398270-4 ; 0-12-398270-7
    Database Catalogue ZB MED Medicine, Health

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  3. Book ; Conference proceedings: Recent advances in autism and related disorders

    Coyle, Joseph T.

    85th annual conference of the ARNMD ; 2 December 2005, New York, NY, USA

    (Clinical neuroscience research ; 6,3/4)

    2006  

    Institution Association for Research in Nervous and Mental Disease
    Author's details guest eds.: Joeph T. Coyle ... Association for Research in Nervous and Mental Disease
    Series title Clinical neuroscience research ; 6,3/4
    Collection
    Language English
    Size S. 111 - 224 : Ill., graph. Darst.
    Publisher Elsevier
    Publishing place Amsterdam u.a.
    Publishing country Netherlands
    Document type Book ; Conference proceedings
    HBZ-ID HT014910385
    Database Catalogue ZB MED Medicine, Health

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  4. Book: Translational neuroscience

    Barrett, James E. / Coyle, Joseph T. / Williams, Michael

    applications in neurology, psychiatry, and neurodevelopmental disorders

    2012  

    Author's details ed. by James E. Barrett ; Joseph T. Coyle ; Michael Williams
    Keywords Nervous System Diseases ; Drug Discovery ; Mental Disorders ; Neurosciences / methods ; Translational Medical Research / methods
    Language English
    Size XI, 366 S. : Ill., graph. Darst.
    Publisher Cambridge Univ. Press
    Publishing place Cambridge
    Publishing country Great Britain
    Document type Book
    Note Includes bibliographical references and index ; The discovery and development of drugs to treat psychiatric disorders : historical perspective / Michael Williams and James E. Barrett -- Translational approaches to the treatment of anxiety disorders / Charles F. Gillespie, Tamara Weiss, and Kerry J. Ressler -- Mood disorders / Jorge A. Quiroz ... [et al.] -- Schizophrenia / Donald C. Goff and Darrick T. Balu -- Addictive disorders / Charles P. O'Brien -- Section summary and perspectives : translational medicine in psychiatry / Joseph T. Coyle -- Historical perspectives on the discovery and development of drugs to treat neurological disorders / Michael Williams and Joseph T. Coyle -- Alzheimer's disease / Donald L. Price ... [et al.] -- Pain therapeutics / Anthony W. Bannon -- Multiple sclerosis / Alfred W. Sandrock Jr. and Richard A. Rudick -- Parkinson's disease / Jiang-Fan Chen -- Amyotrophic lateral sclerosis / Nicholas J. Maragakis -- Epilepsy / Maciej Gasior and Frank Wiegand -- Section summary and perspectives : translational medicine in neurology / James E. Barrett and Joseph T. Coyle -- Historical perspectives on the use of therapeutic agents to treat neurodevelopmental disorders / Kimberly A. Stigler ... [et al.] -- Autism spectrum disorders / Timothy P.L. Roberts ... [et al.] -- Attention deficit hyperactivity disorder / Craig W. Berridge, David M. Devilbiss, and Amy F.T. Arnsten -- Epigenetic mechanisms in central nervous system disorders / Swati Gupta , Ryley Parrish, and Farah D. Lubin -- Section summary and perspectives : neurodevelopmental disorders and regulation of epigenetic changes / James E. Barrett and Joseph T. Coyle -- Promises and challenges of translational research in neuropsychiatry / David L. Braff
    HBZ-ID HT017300575
    ISBN 978-0-521-51976-2 ; 0-521-51976-4
    Database Catalogue ZB MED Medicine, Health

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  5. Article ; Online: Cortical Pyramidal Neurons Show a Selective Loss of New Synapses in Chronic Schizophrenia.

    Coyle, Joseph T

    The American journal of psychiatry

    2017  Volume 174, Issue 6, Page(s) 510–511

    Language English
    Publishing date 2017-06-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 280045-7
    ISSN 1535-7228 ; 0002-953X
    ISSN (online) 1535-7228
    ISSN 0002-953X
    DOI 10.1176/appi.ajp.2017.17030318
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Schizophrenia: Basic and Clinical.

    Coyle, Joseph T

    Advances in neurobiology

    2017  Volume 15, Page(s) 255–280

    Abstract: Schizophrenia is a chronic severe mental disorder characterized by psychosis, cognitive impairments, and social and motivational deficits. It is associated with a progressive loss of cortical volume after onset of psychosis; nevertheless, cortical ... ...

    Abstract Schizophrenia is a chronic severe mental disorder characterized by psychosis, cognitive impairments, and social and motivational deficits. It is associated with a progressive loss of cortical volume after onset of psychosis; nevertheless, cortical atrophy correlates with the cognitive impairments and the negative symptoms but not with the psychosis. The cortical atrophy is not primarily due to neuronal degeneration but rather to neuronal atrophy and loss of glutamatergic synapses. A downregulation of the presynaptic markers for the parvalbumin-expressing GABAergic interneurons that provide recurrent inhibition to cortical pyramidal neurons is another consistent pathologic feature. Antipsychotic drugs continue after 50 years to be the mainstay of treatment although these drugs, with the possible exception of clozapine, have negligible effects on cognition and negative symptoms. Pharmacologic challenge studies, postmortem analyses and a recent sufficiently powered genome-wide association study and copy number variant studies provide compelling evidence that NMDA receptor hypofunction is an important pathophsysiologic feature of schizophrenia. Silencing the gene encoding serine racemase, the enzyme that synthesizes the cortical-limbic NMDA receptor co-agonist, D-serine, replicates the dendritic and GABAergic pathology and cognitive deficits of schizophrenia in mice. Pharmacologic strategies to overcome NMDA receptor hypofunction hold promise of treating the disabling cognitive and negative symptoms.
    MeSH term(s) Animals ; Antipsychotic Agents/therapeutic use ; Atrophy ; Cerebral Cortex/diagnostic imaging ; Cerebral Cortex/pathology ; Cognitive Dysfunction/metabolism ; Cognitive Dysfunction/physiopathology ; Cognitive Dysfunction/psychology ; Disease Models, Animal ; Down-Regulation ; GABAergic Neurons/metabolism ; Humans ; Interneurons/metabolism ; Mice ; Parvalbumins/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Schizophrenia/diagnostic imaging ; Schizophrenia/drug therapy ; Schizophrenia/metabolism ; Schizophrenia/physiopathology ; Schizophrenic Psychology
    Chemical Substances Antipsychotic Agents ; Parvalbumins ; Receptors, N-Methyl-D-Aspartate
    Language English
    Publishing date 2017-07-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ISSN 2190-5215
    ISSN 2190-5215
    DOI 10.1007/978-3-319-57193-5_9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: The Discovery and Characterization of Targeted Perikaryal-Specific Brain Lesions With Excitotoxins.

    Coyle, Joseph T / Schwarcz, Robert

    Frontiers in neuroscience

    2020  Volume 14, Page(s) 927

    Abstract: ... affected only a small number of brain regions, it was not suitable for targeted brain lesions. The Coyle ...

    Abstract The neurotoxic action of glutamic acid was first described by Lucas and Newhouse, who demonstrated neural degeneration in the inner layers of the neonatal mouse retina after systemic treatment with L-glutamate. Olney extended these findings by showing that neuronal degeneration affected other brain structures including neurons within the arcuate nucleus of the hypothalamus and the area postrema, that the lesion spared axons passing through these areas, and that the neurotoxic potency of glutamate analogs correlated with their excitatory potency, resulting in the designation "excitotoxins." As this method affected only a small number of brain regions, it was not suitable for targeted brain lesions. The Coyle laboratory showed that direct injection of the potent glutamate receptor agonist, kainic acid, into the rat striatum caused a rapid degeneration of intrinsic neurons while sparing axons of passage or termination including the unmyelinated dopaminergic terminals. Kainic acid also exhibited this perikaryal-specific and axon-sparing profile when injected into the cerebellum, hippocampus and eye. However, neuronal vulnerability was highly variable, with hippocampal CA3, pyriform cortex and amygdala neurons exhibiting great sensitivity due to kainate's high convulsive activity. In a comparison study, ibotenic acid, a potent glutamatergic agonist isolated from the
    Language English
    Publishing date 2020-09-08
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2411902-7
    ISSN 1662-453X ; 1662-4548
    ISSN (online) 1662-453X
    ISSN 1662-4548
    DOI 10.3389/fnins.2020.00927
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Farewell.

    Coyle, Joseph T

    JAMA psychiatry

    2014  Volume 71, Issue 12, Page(s) 1321–1322

    Language English
    Publishing date 2014-12-1
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2701203-7
    ISSN 2168-6238 ; 2168-622X
    ISSN (online) 2168-6238
    ISSN 2168-622X
    DOI 10.1001/jamapsychiatry.2014.2282
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Glutamate hypothesis in schizophrenia.

    Uno, Yota / Coyle, Joseph T

    Psychiatry and clinical neurosciences

    2019  Volume 73, Issue 5, Page(s) 204–215

    Abstract: Schizophrenia is a chronic and severe psychiatric disorder that has profound impact on an individual's life and on society. Thus, developing more effective therapeutic interventions is essential. Over the past quarter-century, an abundance of evidence ... ...

    Abstract Schizophrenia is a chronic and severe psychiatric disorder that has profound impact on an individual's life and on society. Thus, developing more effective therapeutic interventions is essential. Over the past quarter-century, an abundance of evidence from pharmacologic challenges, post-mortem studies, brain imaging, and genetic studies supports the role of glutamatergic dysregulation in the pathophysiology of schizophrenia, and the results of recent randomized clinical trials based on this evidence have yielded promising results. In this article, we review the evidence that alterations in glutamatergic neurotransmission, especially focusing on the N-methyl-d-aspartate receptor (NMDAR) function, may be a critical causative feature of schizophrenia, how this contributes to pathologic circuit function in the brain, and how these insights are revealing whole new avenues for treatment development that could reduce treatment-resistant symptoms, which account for persistent disability.
    MeSH term(s) Animals ; Glutamic Acid/metabolism ; Humans ; Receptors, N-Methyl-D-Aspartate/metabolism ; Schizophrenia/metabolism
    Chemical Substances Receptors, N-Methyl-D-Aspartate ; Glutamic Acid (3KX376GY7L)
    Language English
    Publishing date 2019-03-06
    Publishing country Australia
    Document type Journal Article ; Review
    ZDB-ID 1292906-2
    ISSN 1440-1819 ; 1323-1316
    ISSN (online) 1440-1819
    ISSN 1323-1316
    DOI 10.1111/pcn.12823
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Fifty Years of Research on Schizophrenia: The Ascendance of the Glutamatergic Synapse.

    Coyle, Joseph T / Ruzicka, W Brad / Balu, Darrick T

    The American journal of psychiatry

    2020  Volume 177, Issue 12, Page(s) 1119–1128

    MeSH term(s) History, 20th Century ; History, 21st Century ; Humans ; Receptors, Glutamate/history ; Receptors, Glutamate/physiology ; Research/history ; Schizophrenia/history ; Schizophrenia/physiopathology ; Synaptic Transmission/physiology
    Chemical Substances Receptors, Glutamate
    Language English
    Publishing date 2020-08-29
    Publishing country United States
    Document type Historical Article ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 280045-7
    ISSN 1535-7228 ; 0002-953X
    ISSN (online) 1535-7228
    ISSN 0002-953X
    DOI 10.1176/appi.ajp.2020.20101481
    Database MEDical Literature Analysis and Retrieval System OnLINE

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