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  1. Book: A tribute to Paul Greengard (1925-2019)

    Greengard, Paul / Zorn, Stevin H.

    (Advances in pharmacology ; volume 90)

    2021  

    Author's details edited by Stevin H. Zorn
    Series title Advances in pharmacology ; volume 90
    Collection
    Language English
    Size xix, 306 Seiten, Illustrationen
    Edition First edition
    Publisher Elsevier Academic Press
    Publishing place Cambridge, MA
    Publishing country United States
    Document type Book
    HBZ-ID HT020883865
    ISBN 978-0-12-822516-5 ; 0-12-822516-5
    Database Catalogue ZB MED Medicine, Health

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  2. Article ; Online: A conversation with Paul Greengard. Interview by Ushma S. Neill.

    Greengard, Paul

    The Journal of clinical investigation

    2013  Volume 123, Issue 3, Page(s) 937–938

    MeSH term(s) England ; History, 20th Century ; History, 21st Century ; Netherlands ; Neurophysiology/history ; Nobel Prize ; United States
    Language English
    Publishing date 2013-03-01
    Publishing country United States
    Document type Autobiography ; Biography ; Historical Article ; Interview ; Portrait
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI68877
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: A conversation with Paul Greengard. Interview by Eric J Nestler.

    Greengard, Paul

    Annual review of pharmacology and toxicology

    2013  Volume 53, Page(s) 1–16

    Abstract: Paul Greengard was born in New York City in 1925. After completing high school, he served three years in the US Navy during World War II and then completed his bachelor's degree at Hamilton College where he majored in physics and mathematics. He obtained ...

    Abstract Paul Greengard was born in New York City in 1925. After completing high school, he served three years in the US Navy during World War II and then completed his bachelor's degree at Hamilton College where he majored in physics and mathematics. He obtained a PhD in biophysics from Johns Hopkins University in 1953 and pursued postdoctoral training with Wilhelm Feldberg at the National Institute for Medical Research in England. After eight years as head of biochemistry at Geigy, and sabbaticals at Albert Einstein College of Medicine and Vanderbilt University, he joined the Yale University faculty as a full professor of pharmacology in 1968. While he was at Yale, Greengard's laboratory performed groundbreaking research, which demonstrated a role for cyclic nucleotides, protein kinases and protein phosphatases, and their protein substrates in the regulation of synaptic transmission. In 1983, Greengard moved to The Rockefeller University, where he has since served as the Vincent Astor Professor and Head of the Laboratory of Molecular and Cellular Neuroscience. Greengard's paradigm-shifting research has continued at Rockefeller and has informed our understanding and possible treatment of a host of brain disorders, including schizophrenia, Alzheimer's disease, Parkinson's disease, and depression. He is the author of more than 950 research articles and reviews. Greengard has received numerous awards and honors, including the Nobel Prize in Physiology or Medicine in 2000, the Metropolitan Life Foundation Award for Medical Research, The National Academy of Sciences Award in Neuroscience, the Ralph W. Gerard Prize in Neuroscience for the Society for Neuroscience, and the Karolinska Institutet's Bicentennial Gold Medal. He is a member of the US National Academy of Sciences and the Institute of Medicine of the National Academies. The following interview was conducted on May 29, 2012.
    MeSH term(s) Animals ; Brain/physiology ; Cyclic AMP/physiology ; Dopamine and cAMP-Regulated Phosphoprotein 32/physiology ; Humans ; Neurons/physiology ; Neuropharmacology
    Chemical Substances Dopamine and cAMP-Regulated Phosphoprotein 32 ; PPP1R1B protein, human ; Cyclic AMP (E0399OZS9N)
    Language English
    Publishing date 2013
    Publishing country United States
    Document type Interview
    ZDB-ID 196587-6
    ISSN 1545-4304 ; 0362-1642
    ISSN (online) 1545-4304
    ISSN 0362-1642
    DOI 10.1146/annurev-pharmtox-062712-160347
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Book: Role of cyclic AMP in cell function

    Greengard, Paul

    (Advances in biochemical psychopharmacology ; 3)

    1970  

    Author's details ed.: Paul Greengard
    Series title Advances in biochemical psychopharmacology ; 3
    Collection
    Language English
    Size 386 S. : Ill.
    Publisher Raven Pr. u.a.
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT004447508
    Database Catalogue ZB MED Medicine, Health

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    Se 13 -3- verfügbar in Königswinter Königswinter

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  5. Article ; Online: Ependymal cells-CSF flow regulates stress-induced depression.

    Seo, Ji-Seon / Mantas, Ioannis / Svenningsson, Per / Greengard, Paul

    Molecular psychiatry

    2021  Volume 26, Issue 12, Page(s) 7308–7315

    Abstract: Major depressive disorder (MDD) is a severe, common mood disorder. While reduced cerebrospinal fluid (CSF) flow adversely affects brain metabolism and fluid balance in the aging population and during development, only indirect evidence links aberrant CSF ...

    Abstract Major depressive disorder (MDD) is a severe, common mood disorder. While reduced cerebrospinal fluid (CSF) flow adversely affects brain metabolism and fluid balance in the aging population and during development, only indirect evidence links aberrant CSF circulation with many diseases including neurological, neurodegenerative, and psychiatric disorders, such as anxiety and depression. Here we show a very high concentration of p11 as a key molecular determinant for depression in ependymal cells, which is significantly decreased in patients with MDD, and in two mouse models of depression induced by chronic stress, such as restraint and social isolation. The loss of p11 in ependymal cells causes disoriented ependymal planar cell polarity (PCP), reduced CSF flow, and depression-like and anxiety-like behaviors. p11 intrinsically controls PCP core genes, which mediates CSF flow. Viral expression of p11 in ependymal cells specifically rescues the pathophysiological and behavioral deficits caused by loss of p11. Taken together, our results identify a new role and a key molecular determinant for ependymal cell-driven CSF flow in mood disorders and suggest a novel strategy for development of treatments for stress-associated neurological, neurodegenerative, and psychiatric disorders.
    MeSH term(s) Aged ; Animals ; Anxiety Disorders ; Depression/metabolism ; Depressive Disorder, Major ; Disease Models, Animal ; Humans ; Mice ; Neuroglia
    Language English
    Publishing date 2021-07-07
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1330655-8
    ISSN 1476-5578 ; 1359-4184
    ISSN (online) 1476-5578
    ISSN 1359-4184
    DOI 10.1038/s41380-021-01202-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Book: CYCLIC NUCLEOTIDES, PHOSPHORYLATED PROTEINS, AND NEURONAL FUNCTION

    Greengard, Paul

    (DISTINGUISHED LECTURE SERIES OF THE SOCIETY OF GENERAL PHYSIOLOGISTS ; 1)

    1978  

    Author's details PAUL GREENGARD
    Series title DISTINGUISHED LECTURE SERIES OF THE SOCIETY OF GENERAL PHYSIOLOGISTS ; 1
    Distinguished lecture series of the Society of General Physiologists
    Collection Distinguished lecture series of the Society of General Physiologists
    Keywords NEURONS / PHYSIOLOGY ; NUCLEOTIDES, CYCLIC / PHYSIOLOGY ; PHOSPHOPROTEINS / METABOLISM
    Size X, 124 S. ; 22 CM
    Publisher RAVEN PRESS
    Publishing place NEW YORK
    Document type Book
    HBZ-ID HT001085195
    ISBN 0-89004-281-0 ; 978-0-89004-281-6
    Database Catalogue ZB MED Medicine, Health

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    1979 B 97 order for loan Magazin

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  7. Article ; Online: The dentate gyrus in depression.

    Umschweif, Gali / Greengard, Paul / Sagi, Yotam

    The European journal of neuroscience

    2019  Volume 53, Issue 1, Page(s) 39–64

    Abstract: Extensive preclinical research has been conducted in recent years to reveal the cell types, neuronal circuits and molecular and morphological changes implicated in the function of the dentate gyrus in depression. This was profoundly facilitated by the ... ...

    Abstract Extensive preclinical research has been conducted in recent years to reveal the cell types, neuronal circuits and molecular and morphological changes implicated in the function of the dentate gyrus in depression. This was profoundly facilitated by the emergence of methods such as gene targeting, neuronal cell activity manipulation, including optogenetics and chemogenetics, and the development of novel RNA sequencing technology and powerful MRI imagers that were used in clinical studies. These advancements provided researchers with the precise skills needed to evaluate the changes in the dentate gyrus structure and cell function in rodent models as well as in brains of depressed and medicated patients. Here, we review these latest findings and discuss the existing gaps in our knowledge of the role of the dentate gyrus in depression and in mediating the response to antidepressant therapies.
    MeSH term(s) Brain ; Dentate Gyrus ; Depression ; Humans ; Neurons ; Optogenetics
    Language English
    Publishing date 2019-12-20
    Publishing country France
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 645180-9
    ISSN 1460-9568 ; 0953-816X
    ISSN (online) 1460-9568
    ISSN 0953-816X
    DOI 10.1111/ejn.14640
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Identification of Neurensin-2 as a novel modulator of emotional behavior.

    Umschweif, Gali / Medrihan, Lucian / Guillén-Samander, Andrés / Wang, Wei / Sagi, Yotam / Greengard, Paul

    Molecular psychiatry

    2021  Volume 26, Issue 7, Page(s) 2872–2885

    Abstract: Among the hallmarks of major depressive disorders (MDD) are molecular, functional, and morphological impairments in the hippocampus. Recent studies suggested a key role for hippocampal GABAergic interneurons both in depression and in the response to its ... ...

    Abstract Among the hallmarks of major depressive disorders (MDD) are molecular, functional, and morphological impairments in the hippocampus. Recent studies suggested a key role for hippocampal GABAergic interneurons both in depression and in the response to its treatments. These interneurons highly express the chromatin-remodeler SMARCA3 which mediates the response to chronic antidepressants in an unknown mechanism. Using cell-type-specific molecular and physiological approaches, we report that SMARCA3 mediates the glutamatergic signaling in interneurons by repressing the expression of the neuronal protein, Neurensin-2. This vesicular protein associates with endosomes and postsynaptic proteins and is highly and selectively expressed in subpopulations of GABAergic interneurons. Upregulation of Neurensin-2 in the hippocampus either by stress, viral overexpression, or by SMARCA3 deletion, results in depressive-like behaviors. In contrast, the deletion of Neurensin-2 confers resilience to stress and induces AMPA receptor localization to synapses. This pathway which bidirectionally affects emotional behavior could be involved in neuropsychiatric disorders, and suggests novel therapeutic approaches.
    MeSH term(s) Depressive Disorder, Major ; Hippocampus ; Humans ; Interneurons ; Neurons ; Synapses
    Language English
    Publishing date 2021-03-19
    Publishing country England
    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 1330655-8
    ISSN 1476-5578 ; 1359-4184
    ISSN (online) 1476-5578
    ISSN 1359-4184
    DOI 10.1038/s41380-021-01058-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Activation of the p11/SMARCA3/Neurensin-2 pathway in parvalbumin interneurons mediates the response to chronic antidepressants.

    Umschweif, Gali / Medrihan, Lucian / McCabe, Kathryn A / Sagi, Yotam / Greengard, Paul

    Molecular psychiatry

    2021  Volume 26, Issue 7, Page(s) 3350–3362

    Abstract: The delayed behavioral response to chronic antidepressants depends on dynamic changes in the hippocampus. It was suggested that the antidepressant protein p11 and the chromatin remodeling factor SMARCA3 mediate this delayed response by inducing ... ...

    Abstract The delayed behavioral response to chronic antidepressants depends on dynamic changes in the hippocampus. It was suggested that the antidepressant protein p11 and the chromatin remodeling factor SMARCA3 mediate this delayed response by inducing transcriptional changes in hippocampal neurons. However, what target genes are regulated by the p11/SMARCA3 complex to mediate the behavioral response to antidepressants, and what cell type mediates these molecular changes remain unknown. Here we report that the p11/SMARCA3 complex represses Neurensin-2 transcription in hippocampal parvalbumin-expressing interneurons after chronic treatment with Selective Serotonin Reuptake Inhibitors (SSRI). The behavioral response to antidepressants requires upregulation of p11, accumulation of SMARCA3 in the cell nucleus, and a consequent repression of Neurensin-2 transcription in these interneurons. We elucidate a functional role for p11/SMARCA3/Neurensin-2 pathway in regulating AMPA-receptor signaling in parvalbumin-expressing interneurons, a function that is enhanced by chronic treatment with SSRIs. These results link SSRIs to dynamic glutamatergic changes and implicate p11/SMARCA3/Neurensin-2 pathway in the development of more specific and efficient therapeutic strategies for neuropsychiatric disorders.
    MeSH term(s) Animals ; Antidepressive Agents/pharmacology ; DNA-Binding Proteins/metabolism ; Hippocampus/metabolism ; Interneurons/drug effects ; Interneurons/metabolism ; Membrane Proteins/metabolism ; Mice, Inbred C57BL ; Parvalbumins/metabolism ; Selective Serotonin Reuptake Inhibitors/pharmacology ; Transcription Factors/metabolism ; Mice
    Chemical Substances Antidepressive Agents ; DNA-Binding Proteins ; Membrane Proteins ; Parvalbumins ; Serotonin Uptake Inhibitors ; Smarca3 protein, mouse ; Transcription Factors
    Language English
    Publishing date 2021-03-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1330655-8
    ISSN 1476-5578 ; 1359-4184
    ISSN (online) 1476-5578
    ISSN 1359-4184
    DOI 10.1038/s41380-021-01059-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Modulation of amyloid precursor protein cleavage by γ-secretase activating protein through phase separation.

    Jin, Chen / Wang, Jiaoni / Wang, Yumeng / Jia, Bojun / Guo, Xuefei / Yang, Guanghui / Xu, Peng / Greengard, Paul / Zhou, Rui / Shi, Yigong

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

    2022  Volume 119, Issue 12, Page(s) e2122292119

    Abstract: Aberrant cleavage of amyloid precursor protein (APP) by γ-secretase is closely associated with Alzheimer’s disease (AD). γ-secretase activating protein (GSAP) specifically promotes γ-secretase–mediated cleavage of APP. However, the underlying mechanism ... ...

    Abstract Aberrant cleavage of amyloid precursor protein (APP) by γ-secretase is closely associated with Alzheimer’s disease (AD). γ-secretase activating protein (GSAP) specifically promotes γ-secretase–mediated cleavage of APP. However, the underlying mechanism remains enigmatic. Here, we demonstrate that the 16-kDa C-terminal fragment of GSAP (GSAP-16K) undergoes phase separation in vitro and forms puncta-like condensates in cells. GSAP-16K exerts dual modulation on γ-secretase cleavage; GSAP-16K in dilute phase increases APP–C-terminal 99-residue fragment (C99) cleavage toward preferred production of β-amyloid peptide 42 (Aβ42), but GSAP-16K condensates reduce APP-C99 cleavage through substrate sequestration. Notably, the Aβ42/Aβ40 ratio is markedly elevated with increasing concentrations of GSAP-16K. GSAP-16K stably associates with APP-C99 through specific sequence elements. These findings mechanistically explain GSAP-mediated modulation of γ-secretase activity that may have ramifications on the development of potential therapeutics.
    MeSH term(s) Alzheimer Disease/metabolism ; Amyloid Precursor Protein Secretases/metabolism ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Humans ; Peptide Fragments/metabolism
    Chemical Substances Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Peptide Fragments ; Amyloid Precursor Protein Secretases (EC 3.4.-)
    Language English
    Publishing date 2022-03-17
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2122292119
    Database MEDical Literature Analysis and Retrieval System OnLINE

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