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  1. Artikel ; Online: Inhibition of protein kinase C signaling protects prefrontal cortex dendritic spines and cognition from the effects of chronic stress.

    Hains, Avis Brennan / Vu, Mai Anh T / Maciejewski, Paul K / van Dyck, Christopher H / Gottron, Melissa / Arnsten, Amy F T

    Proceedings of the National Academy of Sciences of the United States of America

    2009  Band 106, Heft 42, Seite(n) 17957–17962

    Abstract: The prefrontal cortex r regulates behavior, cognition, and emotion by using working memory. Prefrontal functions are impaired by stress exposure. Acute, stress-induced deficits arise from excessive protein kinase C (PKC) signaling, which diminishes ... ...

    Abstract The prefrontal cortex r regulates behavior, cognition, and emotion by using working memory. Prefrontal functions are impaired by stress exposure. Acute, stress-induced deficits arise from excessive protein kinase C (PKC) signaling, which diminishes prefrontal neuronal firing. Chronic stress additionally produces architectural changes, reducing dendritic complexity and spine density of cortico-cortical pyramidal neurons, thereby disrupting excitatory working memory networks. In vitro studies have found that sustained PKC activity leads to spine loss from hippocampal-cultured neurons, suggesting that PKC may contribute to spine loss during chronic stress exposure. The present study tested whether inhibition of PKC with chelerythrine before daily stress would protect prefrontal spines and working memory. We found that inhibition of PKC rescued working memory impairments and reversed distal apical dendritic spine loss in layer II/III pyramidal neurons of rat prelimbic cortex. Greater spine density predicted better cognitive performance, the first direct correlation between pyramidal cell structure and working memory abilities. These findings suggest that PKC inhibitors may be neuroprotective in disorders with dysregulated PKC signaling such as bipolar disorder, schizophrenia, post-traumatic stress disorder, and lead poisoning--conditions characterized by impoverished prefrontal structural and functional integrity.
    Mesh-Begriff(e) Animals ; Atrophy ; Benzophenanthridines/pharmacology ; Cognition/drug effects ; Cognition/physiology ; Dendritic Spines/drug effects ; Dendritic Spines/enzymology ; Dendritic Spines/physiology ; Dendritic Spines/ultrastructure ; Disease Models, Animal ; Humans ; Male ; Memory/drug effects ; Memory/physiology ; Models, Neurological ; Prefrontal Cortex/drug effects ; Prefrontal Cortex/enzymology ; Prefrontal Cortex/physiology ; Protein Kinase C/antagonists & inhibitors ; Protein Kinase C/physiology ; Protein Kinase Inhibitors/pharmacology ; Rats ; Rats, Sprague-Dawley ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Stress, Physiological/drug effects ; Stress, Physiological/physiology ; Stress, Psychological/drug therapy ; Stress, Psychological/enzymology ; Stress, Psychological/pathology ; Stress, Psychological/physiopathology
    Chemische Substanzen Benzophenanthridines ; Protein Kinase Inhibitors ; chelerythrine (E3B045W6X0) ; Protein Kinase C (EC 2.7.11.13)
    Sprache Englisch
    Erscheinungsdatum 2009-09-11
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.0908563106
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Inhibition of protein kinase C signaling protects prefrontal cortex dendritic spines and cognition from the effects of chronic stress

    Hains, Avis Brennan / Vu, Mai Anh T / Maciejewski, Paul K / van Dyck, Christopher H / Gottron, Melissa / Arnsten, Amy F.T

    Proceedings of the National Academy of Sciences of the United States of America. 2009 Oct. 20, v. 106, no. 42

    2009  

    Abstract: The prefrontal cortex r regulates behavior, cognition, and emotion by using working memory. Prefrontal functions are impaired by stress exposure. Acute, stress-induced deficits arise from excessive protein kinase C (PKC) signaling, which diminishes ... ...

    Abstract The prefrontal cortex r regulates behavior, cognition, and emotion by using working memory. Prefrontal functions are impaired by stress exposure. Acute, stress-induced deficits arise from excessive protein kinase C (PKC) signaling, which diminishes prefrontal neuronal firing. Chronic stress additionally produces architectural changes, reducing dendritic complexity and spine density of cortico-cortical pyramidal neurons, thereby disrupting excitatory working memory networks. In vitro studies have found that sustained PKC activity leads to spine loss from hippocampal-cultured neurons, suggesting that PKC may contribute to spine loss during chronic stress exposure. The present study tested whether inhibition of PKC with chelerythrine before daily stress would protect prefrontal spines and working memory. We found that inhibition of PKC rescued working memory impairments and reversed distal apical dendritic spine loss in layer II/III pyramidal neurons of rat prelimbic cortex. Greater spine density predicted better cognitive performance, the first direct correlation between pyramidal cell structure and working memory abilities. These findings suggest that PKC inhibitors may be neuroprotective in disorders with dysregulated PKC signaling such as bipolar disorder, schizophrenia, post-traumatic stress disorder, and lead poisoning--conditions characterized by impoverished prefrontal structural and functional integrity.
    Schlagwörter cell structures ; cognition ; cortex ; in vitro studies ; lead poisoning ; long term effects ; memory ; neurons ; protein kinase C ; rats ; schizophrenia
    Sprache Englisch
    Erscheinungsverlauf 2009-1020
    Umfang p. 17957-17962.
    Erscheinungsort National Academy of Sciences
    Dokumenttyp Artikel
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.0908563106
    Datenquelle NAL Katalog (AGRICOLA)

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  3. Artikel ; Online: Functional evidence implicating a novel TOR1A mutation in idiopathic, late-onset focal dystonia.

    Calakos, Nicole / Patel, Viren D / Gottron, Melissa / Wang, Gaofeng / Tran-Viet, Khan-Nhat / Brewington, Danielle / Beyer, John L / Steffens, David C / Krishnan, Ranga R / Züchner, Stephan

    Journal of medical genetics

    2009  Band 47, Heft 9, Seite(n) 646–650

    Abstract: Background: TOR1A encodes a chaperone-like AAA-ATPase whose Delta GAG (Delta E) mutation is responsible for an early onset, generalised dystonia syndrome. Because of the established role of the TOR1A gene in heritable generalised dystonia (DYT1), a ... ...

    Abstract Background: TOR1A encodes a chaperone-like AAA-ATPase whose Delta GAG (Delta E) mutation is responsible for an early onset, generalised dystonia syndrome. Because of the established role of the TOR1A gene in heritable generalised dystonia (DYT1), a potential genetic contribution of TOR1A to the more prevalent and diverse presentations of late onset, focal dystonia has been suggested.
    Results: A novel TOR1A missense mutation (c.613T-->A, p.F205I) in a patient with late onset, focal dystonia is reported. The mutation occurs in a highly evolutionarily conserved region encoding the AAA-ATPase domain. Expression assays revealed that expression of F205I or Delta E, but not wildtype TOR1A, produced frequent intracellular inclusions.
    Conclusions: A novel, rare TOR1A variant has been identified in an individual with late onset, focal dystonia and evidence provided that the mutation impairs TOR1A function. Together these findings raise the possibility that this novel TOR1A variant may contribute to the expression of dystonia. In light of these findings, a more comprehensive genetic effort is warranted to identify the role of this and other rare TOR1A variants in the expression of late onset, focal dystonia.
    Mesh-Begriff(e) Age of Onset ; Amino Acid Sequence ; Amino Acid Substitution/genetics ; Cell Line ; Dystonic Disorders/epidemiology ; Dystonic Disorders/genetics ; Humans ; Inclusion Bodies/metabolism ; Middle Aged ; Molecular Chaperones/chemistry ; Molecular Chaperones/genetics ; Molecular Sequence Data ; Mutation/genetics
    Chemische Substanzen Molecular Chaperones ; TOR1A protein, human
    Sprache Englisch
    Erscheinungsdatum 2009-12-02
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 220881-7
    ISSN 1468-6244 ; 0022-2593
    ISSN (online) 1468-6244
    ISSN 0022-2593
    DOI 10.1136/jmg.2009.072082
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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