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  1. Article ; Online: CIB2 and CIB3 are auxiliary subunits of the mechanotransduction channel of hair cells.

    Liang, Xiaoping / Qiu, Xufeng / Dionne, Gilman / Cunningham, Christopher L / Pucak, Michele L / Peng, Guihong / Kim, Ye-Hyun / Lauer, Amanda / Shapiro, Lawrence / Müller, Ulrich

    Neuron

    2021  Volume 109, Issue 13, Page(s) 2131–2149.e15

    Abstract: CIB2 is a ... ...

    Abstract CIB2 is a Ca
    MeSH term(s) Animals ; Calcium-Binding Proteins/chemistry ; Calcium-Binding Proteins/physiology ; Crystallography, X-Ray ; HEK293 Cells ; Hair Cells, Auditory/physiology ; Humans ; Kv Channel-Interacting Proteins/chemistry ; Kv Channel-Interacting Proteins/physiology ; Mechanotransduction, Cellular/physiology ; Membrane Proteins/chemistry ; Membrane Proteins/physiology ; Mice, Inbred C57BL ; Mice, Transgenic ; Mice
    Chemical Substances CIB2 protein, human ; CIB3 protein, human ; Calcium-Binding Proteins ; Kv Channel-Interacting Proteins ; Membrane Proteins ; TMC1 protein, human ; TMC2 protein, human
    Language English
    Publishing date 2021-06-05
    Publishing country United States
    Document type 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.
    ZDB-ID 808167-0
    ISSN 1097-4199 ; 0896-6273
    ISSN (online) 1097-4199
    ISSN 0896-6273
    DOI 10.1016/j.neuron.2021.05.007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2496: Show issues Location:
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    Zs.MG 92: Show issues

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  2. Article: Unkind cytokines: current evidence for the potential role of cytokines in immune-mediated depression.

    Pucak, Michele L / Kaplin, Adam I

    International review of psychiatry (Abingdon, England)

    2005  Volume 17, Issue 6, Page(s) 477–483

    Abstract: A great deal of interest has recently become focused on interactions between the nervous and the immune systems, including the potential for alterations in immune function to contribute to various psychiatric and neurologic disorders. Evidence suggests ... ...

    Abstract A great deal of interest has recently become focused on interactions between the nervous and the immune systems, including the potential for alterations in immune function to contribute to various psychiatric and neurologic disorders. Evidence suggests that cytokines may be involved in the development of depression. Immune-mediated mechanisms in the pathophysiology of some types of depression are reviewed from both clinical and animal studies and the difficulties inherent in studying the interplay of these two complex systems in the development of depression are described.
    MeSH term(s) Animals ; Antidepressive Agents/therapeutic use ; Brain/physiology ; Cytokines/blood ; Depressive Disorder/drug therapy ; Depressive Disorder/immunology ; Hippocampus/physiopathology ; Humans ; Hypothalamo-Hypophyseal System/physiopathology ; Lipopolysaccharides/immunology ; Psychoneuroimmunology ; Serotonin/physiology ; Stress, Psychological/complications ; Tumor Necrosis Factor-alpha/physiology
    Chemical Substances Antidepressive Agents ; Cytokines ; Lipopolysaccharides ; Tumor Necrosis Factor-alpha ; Serotonin (333DO1RDJY)
    Language English
    Publishing date 2005-12
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1018090-4
    ISSN 0954-0261
    ISSN 0954-0261
    DOI 10.1080/02646830500381757
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2819: Show issues Location:
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  3. Article: The immune system and neuropsychiatric diseases.

    Kerr, Douglas / Krishnan, Chitra / Pucak, Michele L / Carmen, Jessica

    International review of psychiatry (Abingdon, England)

    2005  Volume 17, Issue 6, Page(s) 443–449

    Abstract: The immune system has a complex and dynamic relationship with the nervous system, both in health and disease. The immune system surveys the central and peripheral nervous systems, becoming activated in response to foreign substances, infectious particles ...

    Abstract The immune system has a complex and dynamic relationship with the nervous system, both in health and disease. The immune system surveys the central and peripheral nervous systems, becoming activated in response to foreign substances, infectious particles or neoplasms. Conversely, the nervous system modulates immune system function both through the neuroendocrine axis and through vagus nerve efferents. In disease states, this dynamic relationship is perturbed, resulting in neuropsychiatric diseases. In this manuscript, we will summarize fundamental principles of the immune system and its interaction with the nervous system. We will describe the critical components of the adaptive and innate branches of the immune system and will describe important effectors and signalling pathways in each. By understanding the principles of the immune system and how these principles relate to nervous system function, the reader will be prepared to interpret subsequent manuscripts in this issue.
    MeSH term(s) Brain/physiopathology ; Cytokines/immunology ; Humans ; Hypothalamo-Hypophyseal System/physiopathology ; Immunity, Innate/immunology ; Infection/immunology ; Neoplasms/immunology ; Nervous System/physiopathology ; Neurosecretory Systems/physiopathology ; Psychoneuroimmunology ; Vagus Nerve/physiopathology
    Chemical Substances Cytokines
    Language English
    Publishing date 2005-12
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1018090-4
    ISSN 0954-0261
    ISSN 0954-0261
    DOI 10.1080/0264830500381435
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2819: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  4. Article: Neuropsychiatric manifestations of depression in multiple sclerosis: neuroinflammatory, neuroendocrine, and neurotrophic mechanisms in the pathogenesis of immune-mediated depression.

    Pucak, Michele L / Carroll, Katherine A L / Kerr, Douglas A / Kaplin, Adam I

    Dialogues in clinical neuroscience

    2007  Volume 9, Issue 2, Page(s) 125–139

    Abstract: Evidence suggests that depression in multiple sclerosis (MS) is largely biologically mediated by some of the same processes involved in the immunopathogenesis of this neurologic disease. In particular, the increase in proinflammatory cytokines, ... ...

    Abstract Evidence suggests that depression in multiple sclerosis (MS) is largely biologically mediated by some of the same processes involved in the immunopathogenesis of this neurologic disease. In particular, the increase in proinflammatory cytokines, activation of the hypothalamic-pituitary-adrenal (HPA) axis, and reduction in neurotrophic factors that occur in MS may each account for the increased rate of depression seen in MS. The possible contributions of these neuroinflammatory, neuroendocrine, and neurotrophic mechanisms suggest a diverse array of novel treatment strategies for depression, both in the context of inflammatory conditions as well as in idiopathic depression. Furthermore, if such processes in MS play a causative role in the pathogenesis of depression, and depression in turn has affects on neurophysiological processes related to immune function, then treatment of depression might have a positive effect on MS disease progression. This makes treating MS depression a neuropsychiatric imperative.
    MeSH term(s) Animals ; Brain/immunology ; Brain/pathology ; Brain/physiopathology ; Cytokines/immunology ; Depressive Disorder/immunology ; Depressive Disorder/physiopathology ; Humans ; Hypothalamo-Hypophyseal System/immunology ; Hypothalamo-Hypophyseal System/physiopathology ; Immune System/physiopathology ; Interferons/adverse effects ; Multiple Sclerosis/complications ; Multiple Sclerosis/immunology ; Multiple Sclerosis/psychology ; Pituitary-Adrenal System/immunology ; Pituitary-Adrenal System/physiopathology ; Stress, Psychological/immunology ; Stress, Psychological/physiopathology ; Stress, Psychological/psychology
    Chemical Substances Cytokines ; Interferons (9008-11-1)
    Language English
    Publishing date 2007
    Publishing country France
    Document type Journal Article ; Review
    ZDB-ID 2188781-0
    ISSN 1294-8322
    ISSN 1294-8322
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6188: Show issues Location:
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  5. Article ; Online: NMDA receptor signaling in oligodendrocyte progenitors is not required for oligodendrogenesis and myelination.

    De Biase, Lindsay M / Kang, Shin H / Baxi, Emily G / Fukaya, Masahiro / Pucak, Michele L / Mishina, Masayoshi / Calabresi, Peter A / Bergles, Dwight E

    The Journal of neuroscience : the official journal of the Society for Neuroscience

    2011  Volume 31, Issue 35, Page(s) 12650–12662

    Abstract: Oligodendrocyte precursor cells (OPCs) express NMDA receptors (NMDARs) and form synapses with glutamatergic neurons throughout the CNS. Although glutamate influences the proliferation and maturation of these progenitors in vitro, the role of NMDAR ... ...

    Abstract Oligodendrocyte precursor cells (OPCs) express NMDA receptors (NMDARs) and form synapses with glutamatergic neurons throughout the CNS. Although glutamate influences the proliferation and maturation of these progenitors in vitro, the role of NMDAR signaling in oligodendrogenesis and myelination in vivo is not known. Here, we investigated the consequences of genetically deleting the obligatory NMDAR subunit NR1 from OPCs and their oligodendrocyte progeny in the CNS of developing and mature mice. NMDAR-deficient OPCs proliferated normally, achieved appropriate densities in gray and white matter, and differentiated to form major white matter tracts without delay. OPCs also retained their characteristic physiological and morphological properties in the absence of NMDAR signaling and were able to form synapses with glutamatergic axons. However, expression of calcium-permeable AMPA receptors (AMPARs) was enhanced in NMDAR-deficient OPCs. These results suggest that NMDAR signaling is not used to control OPC development but to regulate AMPAR-dependent signaling with surrounding axons, pointing to additional functions for these ubiquitous glial cells.
    MeSH term(s) Age Factors ; Aldehyde Dehydrogenase 1 Family ; Analysis of Variance ; Animals ; Animals, Newborn ; Autophagy-Related Proteins ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Biophysics ; Brain/cytology ; Brain/growth & development ; Bromodeoxyuridine/metabolism ; Cell Differentiation/genetics ; Cell Differentiation/physiology ; Cell Proliferation ; Electric Stimulation ; Excitatory Postsynaptic Potentials/drug effects ; Excitatory Postsynaptic Potentials/genetics ; Gene Expression Regulation, Developmental/genetics ; Glial Fibrillary Acidic Protein/metabolism ; Glutamic Acid/metabolism ; Glutamic Acid/pharmacology ; In Vitro Techniques ; Intracellular Signaling Peptides and Proteins/metabolism ; Isoenzymes/metabolism ; Luminescent Proteins/genetics ; Mice ; Mice, Transgenic ; Myelin Basic Protein/metabolism ; Oligodendroglia/metabolism ; Patch-Clamp Techniques ; Receptor, Platelet-Derived Growth Factor alpha/metabolism ; Receptors, Atrial Natriuretic Factor/metabolism ; Receptors, N-Methyl-D-Aspartate/deficiency ; Receptors, N-Methyl-D-Aspartate/metabolism ; Retinal Dehydrogenase/metabolism ; Signal Transduction/genetics ; Signal Transduction/physiology ; Stem Cells/physiology ; Synapses/genetics ; Synapses/physiology
    Chemical Substances Autophagy-Related Proteins ; Basic Helix-Loop-Helix Transcription Factors ; Glial Fibrillary Acidic Protein ; Intracellular Signaling Peptides and Proteins ; Isoenzymes ; Luminescent Proteins ; Myelin Basic Protein ; NR1 NMDA receptor ; Olig1 protein, mouse ; Rb1cc1 protein, mouse ; Receptors, N-Methyl-D-Aspartate ; Glutamic Acid (3KX376GY7L) ; Aldehyde Dehydrogenase 1 Family (EC 1.2.1) ; ALDH1A1 protein, mouse (EC 1.2.1.36) ; Retinal Dehydrogenase (EC 1.2.1.36) ; Receptor, Platelet-Derived Growth Factor alpha (EC 2.7.10.1) ; Receptors, Atrial Natriuretic Factor (EC 4.6.1.2) ; atrial natriuretic factor receptor C (EC 4.6.1.2) ; Bromodeoxyuridine (G34N38R2N1)
    Language English
    Publishing date 2011-08-31
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 604637-x
    ISSN 1529-2401 ; 0270-6474
    ISSN (online) 1529-2401
    ISSN 0270-6474
    DOI 10.1523/JNEUROSCI.2455-11.2011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1668: Show issues Location:
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