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  1. Article: A Putative Role for Ubiquitin-Proteasome Signaling in Estrogenic Memory Regulation.

    Beamish, Sarah B / Frick, Karyn M

    Frontiers in behavioral neuroscience

    2022  Volume 15, Page(s) 807215

    Abstract: Sex steroid hormones such as 17β-estradiol ( ... ...

    Abstract Sex steroid hormones such as 17β-estradiol (E
    Language English
    Publishing date 2022-01-25
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2452960-6
    ISSN 1662-5153
    ISSN 1662-5153
    DOI 10.3389/fnbeh.2021.807215
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: G protein-coupled estrogen receptor (GPER) in the dorsal hippocampus regulates memory consolidation in gonadectomized male mice, likely via different signaling mechanisms than in female mice.

    Machado, Gustavo D B / Schnitzler, Alexis L / Fleischer, Aaron W / Beamish, Sarah B / Frick, Karyn M

    Hormones and behavior

    2024  Volume 161, Page(s) 105516

    Abstract: Studies in ovariectomized (OVX) female rodents suggest that G protein-coupled estrogen receptor (GPER) is a key regulator of memory, yet little is known about its importance to memory in males or the cellular mechanisms underlying its mnemonic effects in ...

    Abstract Studies in ovariectomized (OVX) female rodents suggest that G protein-coupled estrogen receptor (GPER) is a key regulator of memory, yet little is known about its importance to memory in males or the cellular mechanisms underlying its mnemonic effects in either sex. In OVX mice, bilateral infusion of the GPER agonist G-1 into the dorsal hippocampus (DH) enhances object recognition and spatial memory consolidation in a manner dependent on rapid activation of c-Jun N-terminal kinase (JNK) signaling, cofilin phosphorylation, and actin polymerization in the DH. However, the effects of GPER on memory consolidation and DH cell signaling in males are unknown. Thus, the present study first assessed effects of DH infusion of G-1 or the GPER antagonist G-15 on object recognition and spatial memory consolidation in gonadectomized (GDX) male mice. As in OVX mice, immediate post-training bilateral DH infusion of G-1 enhanced, whereas G-15 impaired, memory consolidation in the object recognition and object placement tasks. However, G-1 did not increase levels of phosphorylated JNK (p46, p54) or cofilin in the DH 5, 15, or 30 min after infusion, nor did it affect phosphorylation of ERK (p42, p44), PI3K, or Akt. Levels of phospho-cAMP-responsive element binding protein (CREB) were elevated in the DH 30 min following G-1 infusion, indicating that GPER in males activates a yet unknown signaling mechanism that triggers CREB-mediated gene transcription. Our findings show for the first time that GPER in the DH regulates memory consolidation in males and suggests sex differences in underlying signaling mechanisms.
    MeSH term(s) Animals ; Male ; Memory Consolidation/physiology ; Memory Consolidation/drug effects ; Female ; Mice ; Hippocampus/metabolism ; Hippocampus/drug effects ; Receptors, G-Protein-Coupled/metabolism ; Signal Transduction/physiology ; Signal Transduction/drug effects ; Receptors, Estrogen/metabolism ; Ovariectomy ; Orchiectomy ; Cyclopentanes/pharmacology ; Cyclic AMP Response Element-Binding Protein/metabolism ; Mice, Inbred C57BL ; Quinolines
    Chemical Substances Receptors, G-Protein-Coupled ; GPER1 protein, mouse ; Receptors, Estrogen ; 1-(4-(6-bromobenzo(1,3)dioxol-5-yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta(c)quinolin-8-yl)ethanone ; Cyclopentanes ; Cyclic AMP Response Element-Binding Protein ; Quinolines
    Language English
    Publishing date 2024-03-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 214409-8
    ISSN 1095-6867 ; 0018-506X
    ISSN (online) 1095-6867
    ISSN 0018-506X
    DOI 10.1016/j.yhbeh.2024.105516
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 693: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: The effects of early-life immune activation on microglia-mediated neuronal remodeling and the associated ontogeny of hippocampal-dependent learning in juvenile rats.

    Osborne, Brittany F / Beamish, Sarah B / Schwarz, Jaclyn M

    Brain, behavior, and immunity

    2021  Volume 96, Page(s) 239–255

    Abstract: Many neurodevelopmental disorders and associated learning deficits have been linked to early-life immune activation or ongoing immune dysregulation (Laskaris et al., 2016; O'Connor et al., 2014; Frick et al., 2013). Neuroscientists have begun to ... ...

    Abstract Many neurodevelopmental disorders and associated learning deficits have been linked to early-life immune activation or ongoing immune dysregulation (Laskaris et al., 2016; O'Connor et al., 2014; Frick et al., 2013). Neuroscientists have begun to understand how the maturation of neural circuits allows for the emergence of cognitive and learning behaviors; yet we know very little about how these developing neural circuits are perturbed by certain events, including risk-factors such as early-life immune activation and immune dysregulation. To answer these questions, we examined the impact of early-life immune activation on the emergence of hippocampal-dependent learning in juvenile male and female rats using a well-characterized hippocampal-dependent learning task and we investigated the corresponding, dynamic multicellular interactions in the hippocampus that may contribute to these learning deficits. We found that even low levels of immune activation can result in hippocampal-depedent learning deficits days later, but only when this activation occurs during a sensitive period of development. The initial immune response and associated cytokine production in the hippocampus resolved within 24 h, several days prior to the observed learning deficit, but notably the initial immune response was followed by altered microglial-neuronal communication and synapse remodeling that changed the structure of hippocampal neurons during this period of juvenile brain development. We conclude that immune activation or dysregulation during a sensitive period of hippocampal development can precipitate the emergence of learning deficits via a multi-cellular process that may be initiated by, but not the direct result of the initial cytokine response. SIGNIFICANCE STATEMENT: Many neurodevelopmental disorders have been linked to early-life immune activation or immune dysregulation; however, very little is known about how dynamic changes in neuroimmune cells mediate the transition from normal brain function to the early stages of cognitive disorders, or how changes in immune signaling are subsequently integrated into developing neuronal networks. The current experiments examined the consequences of immune activation on the cellular and molecular changes that accompany the emergence of learning deficits during a sensitive period of hippocampal development. These findings have the potential to significantly advance our understanding of how early-life immune activation or dysregulation can result in the emergence of cognitive and learning deficits that are the largest source of years lived with disability in humans.
    MeSH term(s) Animals ; Female ; Hippocampus ; Male ; Microglia ; Neuronal Plasticity ; Neurons ; Rats ; Synapses
    Language English
    Publishing date 2021-06-11
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 639219-2
    ISSN 1090-2139 ; 0889-1591
    ISSN (online) 1090-2139
    ISSN 0889-1591
    DOI 10.1016/j.bbi.2021.06.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2276: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 327: Show issues

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  4. Article ; Online: Sex differences in training-induced activity of the ubiquitin proteasome system in the dorsal hippocampus and medial prefrontal cortex of male and female mice.

    Beamish, Sarah B / Gross, Kellie S / Anderson, McKenna M / Helmstetter, Fred J / Frick, Karyn M

    Learning & memory (Cold Spring Harbor, N.Y.)

    2022  Volume 29, Issue 9, Page(s) 302–311

    Abstract: The ubiquitin proteasome system (UPS) is a primary mechanism through which proteins are degraded in cells. UPS activity in the dorsal hippocampus (DH) is necessary for multiple types of memory, including object memory, in male rodents. However, sex ... ...

    Abstract The ubiquitin proteasome system (UPS) is a primary mechanism through which proteins are degraded in cells. UPS activity in the dorsal hippocampus (DH) is necessary for multiple types of memory, including object memory, in male rodents. However, sex differences in DH UPS activation after fear conditioning suggest that other forms of learning may also differentially regulate DH UPS activity in males and females. Here, we examined markers of UPS activity in the synaptic and cytoplasmic fractions of DH and medial prefrontal cortex (mPFC) tissue collected 1 h following object training. In males, training increased phosphorylation of proteasomal subunit Rpt6, 20S proteasome activity, and the amount of PSD-95 in the DH synaptic fraction, as well as proteasome activity in the mPFC synaptic fraction. In females, training did not affect measures of UPS or synaptic activity in the DH synaptic fraction or in either mPFC fraction but increased Rpt6 phosphorylation in the DH cytoplasmic fraction. Overall, training-induced UPS activity was greater in males than in females, greater in the DH than in the mPFC, and greater in synaptic fractions than in cytosol. These data suggest that object training drives sex-specific alterations in UPS activity across brain regions and subcellular compartments important for memory.
    MeSH term(s) Animals ; Conditioning, Classical/physiology ; Female ; Hippocampus/physiology ; Male ; Mice ; Prefrontal Cortex/physiology ; Proteasome Endopeptidase Complex/metabolism ; Sex Characteristics ; Ubiquitin/metabolism
    Chemical Substances Ubiquitin ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
    Language English
    Publishing date 2022-09-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1204777-6
    ISSN 1549-5485 ; 1072-0502
    ISSN (online) 1549-5485
    ISSN 1072-0502
    DOI 10.1101/lm.053492.121
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4107: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Development of a Novel, Small-Molecule Brain-Penetrant Histone Deacetylase Inhibitor That Enhances Spatial Memory Formation in Mice.

    Belayet, Jawad B / Beamish, Sarah / Rahaman, Mizzanoor / Alanani, Samer / Virdi, Rajdeep S / Frick, David N / Rahman, A F M Towheedur / Ulicki, Joseph S / Biswas, Sreya / Arnold, Leggy A / Roni, M S Rashid / Cheng, Eric Y / Steeber, Douglas A / Frick, Karyn M / Hossain, M Mahmun

    Journal of medicinal chemistry

    2022  Volume 65, Issue 4, Page(s) 3388–3403

    Abstract: Histone acetylation is a prominent epigenetic modification linked to the memory loss symptoms associated with neurodegenerative disease. The use of existing histone deacetylase inhibitor (HDACi) drugs for treatment is precluded by their weak blood-brain ... ...

    Abstract Histone acetylation is a prominent epigenetic modification linked to the memory loss symptoms associated with neurodegenerative disease. The use of existing histone deacetylase inhibitor (HDACi) drugs for treatment is precluded by their weak blood-brain barrier (BBB) permeability and undesirable toxicity. Here, we address these shortcomings by developing a new class of disulfide-based compounds, inspired by the scaffold of the FDA-approved HDACi romidepsin (FK288). Our findings indicate that our novel compound MJM-1 increases the overall level of histone 3 (H3) acetylation in a prostate cancer cell line. In mice, MJM-1 injected intraperitoneally (i.p.) crossed the BBB and could be detected in the hippocampus, a brain region that mediates memory. Consistent with this finding, we found that the post-training i.p. administration of MJM-1 enhanced hippocampus-dependent spatial memory consolidation in male mice. Therefore, MJM-1 represents a potential lead for further optimization as a therapeutic strategy for ameliorating cognitive deficits in aging and neurodegenerative diseases.
    MeSH term(s) Animals ; Brain/metabolism ; Cell Line, Tumor ; Histone Deacetylase Inhibitors/chemical synthesis ; Histone Deacetylase Inhibitors/pharmacokinetics ; Histone Deacetylase Inhibitors/pharmacology ; Mice ; Mice, Inbred BALB C ; Spatial Memory/drug effects
    Chemical Substances Histone Deacetylase Inhibitors
    Language English
    Publishing date 2022-02-08
    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 218133-2
    ISSN 1520-4804 ; 0022-2623
    ISSN (online) 1520-4804
    ISSN 0022-2623
    DOI 10.1021/acs.jmedchem.1c01928
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.B 151: Show issues Location:
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    Zs.MB 1: Show issues

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