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The glutamate transporter EAAT2 is transiently expressed in developing human cerebral white matter.

The glutamate transporter EAAT2 is transiently expressed in developing human cerebral white matter. Research Abstract Details 

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  • The glutamate transporter EAAT2 is transiently expressed in developing human cerebral white matter. Abstract Text:

    tara m desilvaTara M Desilva,hannah c kinneyHannah C Kinney,natalia s borensteinNatalia S Borenstein,felicia l trachtenbergFelicia L Trachtenberg,nina irwinNina Irwin,joseph j volpeJoseph J Volpe,paul a rosenbergPaul A Rosenberg,

    The major brain abnormality underlying cerebral palsy in premature infants is periventricular leukomalacia (PVL), a lesion of the immature cerebral white matter. Oligodendrocyte precursors (pre-OLs; O4(+)O1(-)) predominate in human cerebral white matter during the peak time frame for PVL (24-32 gestational weeks) and are vulnerable to excitotoxicity. We hypothesize that PVL reflects, in part, excitotoxicity to pre-OLs resulting from cerebral ischemia/reperfusion. Reversal of glutamate transport in the setting of energy failure is a major source of pathologic accumulation of extracellular glutamate. Here, we identify and localize the glutamate transporters in human cerebral white matter during the age range of PVL. In situ hybridization was performed with digoxigenin-labeled probes directed against the full-length coding regions of EAAT1, EAAT2, and EAAT3. EAAT2 mRNA was abundant in human fetal white matter during the period of peak incidence of PVL and virtually disappeared by 2 postnatal months. Its developmental profile differed significantly from that of both EAAT1 and EAAT3 mRNA. Immunoblotting demonstrated that EAAT2 protein was highly expressed in early development relative to adult values. Double-label immunocytochemistry detected EAAT2 in OLs but not astrocytes or axons in the human fetal white matter. We conclude that transient expression of EAAT2 occurs during the window of peak vulnerability for PVL, suggesting that this developmentally up-regulated transporter may be a major source of extracellular glutamate in ischemic injury to the cerebral white matter of the preterm infant.

    The glutamate transporter EAAT2 is transiently expressed in developing human cerebral white matter. Publishing Authors By Initials

    tm desilvaTM Desilva,hc kinneyHC Kinney,ns borensteinNS Borenstein,fl trachtenbergFL Trachtenberg,n irwinN Irwin,jj volpeJJ Volpe,pa rosenbergPA Rosenberg,

    For similar biochemical phenomena, metabolism, and nutrition: metabolism: pharmacokinetics: tissue distribution research abstracts see: biochemical phenomena, metabolism, and nutrition: metabolism: pharmacokinetics: tissue distribution research

    PUBMED ID PMID:

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    The glutamate transporter EAAT2 is transiently expressed in developing human cerebral white matter. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: The Journal of comparative neurology

    VOLUME: 501

    Page Numbers: 879-90

    Journal Abbreviation: J. Comp. Neurol.

    ISSN: 0021-9967

    DAY: 20

    MONTH: Apr

    YEAR: 2007

    The glutamate transporter EAAT2 is transiently expressed in developing human cerebral white matter. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 406041

    The glutamate transporter EAAT2 is transiently expressed in developing human cerebral white matter. Keywords Mesh Terms:

    KEYWORDS: Tissue Distribution

    MESH TERMS: analysis

    Chemical & Substance for Abstract: The glutamate transporter EAAT2 is transiently expressed in developing human cerebral white matter. Information

    Substance Name: RNA, Messenger

    Registry Number: 0

    Grant and Affiliation Information for The glutamate transporter EAAT2 is transiently expressed in developing human cerebral white matter.

    AFFILIATION: Neurobiology Program, Children's Hospital Boston, Department of Neurology, Harvard Medical School, Boston, Massachusetts 02115, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NINDS

    GRANT: NS41883

    ACRONYM: NS

    MEDLINETA: J Comp Neurol

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