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  1. Article: Chronic Stimulation of Alpha-2A-Adrenoceptors With Guanfacine Protects Rodent Prefrontal Cortex Dendritic Spines and Cognition From the Effects of Chronic Stress.

    Hains, Avis Brennan / Yabe, Yoko / Arnsten, Amy F T

    Neurobiology of stress

    2015  Volume 2, Page(s) 1–9

    Abstract: The prefrontal cortex (PFC) provides top-down regulation of behavior, cognition, and emotion, including spatial working memory. However, these PFC abilities are greatly impaired by exposure to acute or chronic stress. Chronic stress exposure in rats ... ...

    Abstract The prefrontal cortex (PFC) provides top-down regulation of behavior, cognition, and emotion, including spatial working memory. However, these PFC abilities are greatly impaired by exposure to acute or chronic stress. Chronic stress exposure in rats induces atrophy of PFC dendrites and spines that correlates with working memory impairment. As similar PFC grey matter loss appears to occur in mental illness, the mechanisms underlying these changes need to be better understood. Acute stress exposure impairs PFC cognition by activating feedforward cAMP-calcium-K
    Language English
    Publishing date 2015-02-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2816500-7
    ISSN 2352-2895
    ISSN 2352-2895
    DOI 10.1016/j.ynstr.2015.01.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; 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  Volume 106, Issue 42, Page(s) 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 term(s) 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
    Chemical Substances Benzophenanthridines ; Protein Kinase Inhibitors ; chelerythrine (E3B045W6X0) ; Protein Kinase C (EC 2.7.11.13)
    Language English
    Publishing date 2009-09-11
    Publishing country United States
    Document type 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: 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.
    Keywords cell structures ; cognition ; cortex ; in vitro studies ; lead poisoning ; long term effects ; memory ; neurons ; protein kinase C ; rats ; schizophrenia
    Language English
    Dates of publication 2009-1020
    Size p. 17957-17962.
    Publishing place National Academy of Sciences
    Document type Article
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.0908563106
    Database NAL-Catalogue (AGRICOLA)

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