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  1. Article: Effects of chronic lithium treatment on neuronal excitability and GABAergic transmission in an

    Caballero-Florán, René N / Nelson, Andrew D / Min, Lia / Jenkins, Paul M

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Bipolar disorder (BD) is a common psychiatric disease that can lead to psychosocial disability, decreased quality of life, and high risk for suicide. Genome-wide association studies have shown that ... ...

    Abstract Bipolar disorder (BD) is a common psychiatric disease that can lead to psychosocial disability, decreased quality of life, and high risk for suicide. Genome-wide association studies have shown that the
    Language English
    Publishing date 2023-10-30
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.10.26.564203
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Synaptotagmin-7 facilitates acetylcholine release in splanchnic nerve-chromaffin cell synapses during nerve activity.

    Caballero-Florán, René N / Bendahmane, Mounir / Gupta, Julie P / Chen, Xiaohuan / Wu, Xiaojun / Morales, Alina / Anantharam, Arun / Jenkins, Paul M

    Neuroscience letters

    2023  Volume 800, Page(s) 137129

    Abstract: Disturbances that threaten homeostasis elicit activation of the sympathetic nervous system (SNS) and the adrenal medulla. The effectors discharge as a unit to drive global and immediate changes in whole-body physiology. Descending sympathetic information ...

    Abstract Disturbances that threaten homeostasis elicit activation of the sympathetic nervous system (SNS) and the adrenal medulla. The effectors discharge as a unit to drive global and immediate changes in whole-body physiology. Descending sympathetic information is conveyed to the adrenal medulla via preganglionic splanchnic fibers. These fibers pass into the gland and synapse onto chromaffin cells, which synthesize, store, and secrete catecholamines and vasoactive peptides. While the importance of the sympatho-adrenal branch of the autonomic nervous system has been appreciated for many decades, the mechanisms underlying transmission between presynaptic splanchnic neurons and postsynaptic chromaffin cells have remained obscure. In contrast to chromaffin cells, which have enjoyed sustained attention as a model system for exocytosis, even the Ca
    MeSH term(s) Acetylcholine/metabolism ; Synaptotagmins/metabolism ; Splanchnic Nerves/metabolism ; Chromaffin Cells/metabolism ; Adrenal Medulla/metabolism ; Synapses/physiology
    Chemical Substances Acetylcholine (N9YNS0M02X) ; Synaptotagmins (134193-27-4)
    Language English
    Publishing date 2023-02-14
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 194929-9
    ISSN 1872-7972 ; 0304-3940
    ISSN (online) 1872-7972
    ISSN 0304-3940
    DOI 10.1016/j.neulet.2023.137129
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1166: 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: Physical and functional convergence of the autism risk genes Scn2a and Ank2 in neocortical pyramidal cell dendrites.

    Nelson, Andrew D / Catalfio, Amanda M / Gupta, Julie P / Min, Lia / Caballero-Florán, René N / Dean, Kendall P / Elvira, Carina C / Derderian, Kimberly D / Kyoung, Henry / Sahagun, Atehsa / Sanders, Stephan J / Bender, Kevin J / Jenkins, Paul M

    Neuron

    2024  Volume 112, Issue 7, Page(s) 1133–1149.e6

    Abstract: Dysfunction in sodium channels and their ankyrin scaffolding partners have both been implicated in neurodevelopmental disorders, including autism spectrum disorder (ASD). In particular, the genes SCN2A, which encodes the sodium channel ... ...

    Abstract Dysfunction in sodium channels and their ankyrin scaffolding partners have both been implicated in neurodevelopmental disorders, including autism spectrum disorder (ASD). In particular, the genes SCN2A, which encodes the sodium channel Na
    MeSH term(s) Animals ; Mice ; Ankyrins/genetics ; Ankyrins/metabolism ; Autism Spectrum Disorder/genetics ; Autism Spectrum Disorder/metabolism ; Autistic Disorder/metabolism ; Dendrites/physiology ; NAV1.2 Voltage-Gated Sodium Channel/genetics ; Neocortex/metabolism ; Pyramidal Cells/physiology
    Chemical Substances Ankyrins ; NAV1.2 Voltage-Gated Sodium Channel ; Scn2a protein, mouse ; Ank2 protein, mouse
    Language English
    Publishing date 2024-01-29
    Publishing country United States
    Document type Journal Article
    ZDB-ID 808167-0
    ISSN 1097-4199 ; 0896-6273
    ISSN (online) 1097-4199
    ISSN 0896-6273
    DOI 10.1016/j.neuron.2024.01.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2496: 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.MG 92: Show issues

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  4. Article ; Online: DSCAM gene triplication causes excessive GABAergic synapses in the neocortex in Down syndrome mouse models.

    Liu, Hao / Caballero-Florán, René N / Hergenreder, Ty / Yang, Tao / Hull, Jacob M / Pan, Geng / Li, Ruonan / Veling, Macy W / Isom, Lori L / Kwan, Kenneth Y / Huang, Z Josh / Fuerst, Peter G / Jenkins, Paul M / Ye, Bing

    PLoS biology

    2023  Volume 21, Issue 4, Page(s) e3002078

    Abstract: Down syndrome (DS) is caused by the trisomy of human chromosome 21 (HSA21). A major challenge in DS research is to identify the HSA21 genes that cause specific symptoms. Down syndrome cell adhesion molecule (DSCAM) is encoded by a HSA21 gene. Previous ... ...

    Abstract Down syndrome (DS) is caused by the trisomy of human chromosome 21 (HSA21). A major challenge in DS research is to identify the HSA21 genes that cause specific symptoms. Down syndrome cell adhesion molecule (DSCAM) is encoded by a HSA21 gene. Previous studies have shown that the protein level of the Drosophila homolog of DSCAM determines the size of presynaptic terminals. However, whether the triplication of DSCAM contributes to presynaptic development in DS remains unknown. Here, we show that DSCAM levels regulate GABAergic synapses formed on neocortical pyramidal neurons (PyNs). In the Ts65Dn mouse model for DS, where DSCAM is overexpressed due to DSCAM triplication, GABAergic innervation of PyNs by basket and chandelier interneurons is increased. Genetic normalization of DSCAM expression rescues the excessive GABAergic innervations and the increased inhibition of PyNs. Conversely, loss of DSCAM impairs GABAergic synapse development and function. These findings demonstrate excessive GABAergic innervation and synaptic transmission in the neocortex of DS mouse models and identify DSCAM overexpression as the cause. They also implicate dysregulated DSCAM levels as a potential pathogenic driver in related neurological disorders.
    MeSH term(s) Animals ; Humans ; Mice ; Disease Models, Animal ; Down Syndrome/genetics ; Down Syndrome/metabolism ; Down Syndrome/pathology ; Drosophila ; Interneurons/metabolism ; Neocortex ; Presynaptic Terminals/metabolism ; Synapses/metabolism
    Chemical Substances Dscam protein, mouse
    Language English
    Publishing date 2023-04-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2126776-5
    ISSN 1545-7885 ; 1544-9173
    ISSN (online) 1545-7885
    ISSN 1544-9173
    DOI 10.1371/journal.pbio.3002078
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6193: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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