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Glutamate-induced exocytosis of glutamate from astrocytes.

Glutamate-induced exocytosis of glutamate from astrocytes. Research Abstract Details 

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  • Glutamate-induced exocytosis of glutamate from astrocytes. Abstract Text:

    jun xuJun Xu,hong pengHong Peng,ning kangNing Kang,zhuo zhaoZhuo Zhao,jane h-c linJane H-C Lin,patric k stantonPatric K Stanton,jian kangJian Kang,

    Recent studies indicate that astrocytes can play a much more active role in neuronal circuits than previously believed, by releasing neurotransmitters such as glutamate and ATP. Here we report that local application of glutamate or glutamine synthetase inhibitors induces astrocytic release of glutamate, which activates a slowly decaying transient inward current (SIC) in CA1 pyramidal neurons and a transient inward current in astrocytes in hippocampal slices. The occurrence of SICs was accompanied by an appearance of large vesicles around the puffing pipette. The frequency of SICs was positively correlated with [glutamate]o. EM imaging of anti-glial fibrillary acid protein-labeled astrocytes showed glutamate-induced large astrocytic vesicles. Imaging of FM 1-43 fluorescence using two-photon laser scanning microscopy detected glutamate-induced formation and fusion of large vesicles identified as FM 1-43-negative structures. Fusion of large vesicles, monitored by collapse of vesicles with a high intensity FM 1-43 stain in the vesicular membrane, coincided with SICs. Glutamate induced two types of large vesicles with high and low intravesicular [Ca2+]. The high [Ca2+] vesicle plays a major role in astrocytic release of glutamate. Vesicular fusion was blocked by infusing the Ca2+ chelator, 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, or the SNARE blocker, tetanus toxin, suggesting Ca2+- and SNARE-dependent fusion. Infusion of the vesicular glutamate transport inhibitor, Rose Bengal, reduced astrocytic glutamate release, suggesting the involvement of vesicular glutamate transports in vesicular transport of glutamate. Our results demonstrate that local [glutamate]o increases induce formation and exocytotic fusion of glutamate-containing large astrocytic vesicles. These large vesicles could play important roles in the feedback control of neuronal circuits and epileptic seizures.

    Glutamate-induced exocytosis of glutamate from astrocytes. Publishing Authors By Initials

    j xuJ Xu,h pengH Peng,n kangN Kang,z zhaoZ Zhao,jh linJH Lin,pk stantonPK Stanton,j kangJ Kang,

    For similar proteins: membrane proteins: membrane fusion proteins: snare proteins research abstracts see: proteins: membrane proteins: membrane fusion proteins: snare proteins research

    PUBMED ID PMID:

    MEDLINE DATE:

    Glutamate-induced exocytosis of glutamate from astrocytes. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: The Journal of biological chemistry

    VOLUME: 282

    Page Numbers: 24185-97

    Journal Abbreviation: J. Biol. Chem.

    ISSN: 0021-9258

    DAY: 21

    MONTH: 06

    YEAR: 2007

    Glutamate-induced exocytosis of glutamate from astrocytes. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 2985121

    Glutamate-induced exocytosis of glutamate from astrocytes. Keywords Mesh Terms:

    KEYWORDS: SNARE Proteins

    MESH TERMS: physiology

    Chemical & Substance for Abstract: Glutamate-induced exocytosis of glutamate from astrocytes. Information

    Substance Name: Calcium

    Registry Number: 7440-70-2

    Grant and Affiliation Information for Glutamate-induced exocytosis of glutamate from astrocytes.

    AFFILIATION: Center for Basic Neuroscience, Department of Molecular Genetics, and Howard Hughes Medical Institutes, University of Texas Southwestern Medical Center, Dallas Texas 75390, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NINDS

    GRANT: NS 39997

    ACRONYM: NS

    MEDLINETA: J Biol Chem

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

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