Excitatory amino acid receptors in glial progenitor cells: Molecular and functional properties

Gallo, Vittorio; Patneau, Doris K.; Mayer, Mark L.; Vaccarino, Flora M.

doi:10.1002/glia.440110204

Cited by 98 publications

(72 citation statements)

References 50 publications

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“…Cases were collected from the autopsy services of the Departments of Pathology of Children's Hospital and Brigham and Women's Hospital, Boston, with permission according to approved hospital research protocols. OLs in white matter were labeled with the pre-OL surface marker O4 (Gard and Pfeiffer, 1990;Back et al, 2002) and double-labeled for GluR4 (Wenthold et al, 1992), which is the AMPA receptor subunit that is expressed consistently by pre-OLs in rodents (Gallo et al, 1994;Patneau et al, 1994;Itoh et al, 2002;Liu et al, 2002). Previous studies demonstrate that the O4 Ab labels the pre-OLs that are prevalent in white matter during gestational weeks 17-32 in the human (Kinney and Back, 1998;Back et al, 2001).…”

Section: Resultsmentioning

confidence: 99%

“…Glutamate accumulates in brain under hypoxic-ischemic conditions (Benveniste et al, 1984;Andine et al, 1991;Hagberg, 1992), and excessive activation of GluRs on neurons is a major mechanism in hypoxic-ischemic neuronal death (Choi, 1992;Hagberg et al, 1994). Rodent pre-OLs express ionotropic GluRs of the AMPA and kainate but not the NMDA subtypes (Gallo et al, 1994;Patneau et al, 1994;. AMPA-kainate receptor antagonists or OGD induces Ca 2ϩ -mediated excitotoxicity in pre-OLs more readily than in mature OLs (Fern and Moller, 2000;Yoshioka et al, 2000;Deng et al, 2003), and this increased vulnerability correlates with transient overexpression of GluRs in pre-OLs compared with mature OLs, both in vitro (Itoh et al, 2002;Rosenberg et al, 2003) and in vivo (Ong et al, 1996;Follett et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Glutamate Receptor-Mediated Oligodendrocyte Toxicity in Periventricular Leukomalacia: A Protective Role for Topiramate

et al. 2004

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Periventricular leukomalacia is a form of hypoxic-ischemic cerebral white matter injury seen most commonly in premature infants and is the major antecedent of cerebral palsy. Glutamate receptor-mediated excitotoxicity is a predominant mechanism of hypoxic-ischemic injury to developing cerebral white matter. We have demonstrated previously the protective effect of AMPA-kainate-type glutamate receptor blockade in a rodent model of periventricular leukomalacia. The present study explores the therapeutic potential of glutamate receptor blockade for hypoxic-ischemic white matter injury. We demonstrate that AMPA receptors are expressed on developing human oligodendrocytes that populate fetal white matter at 23-32 weeks gestation, the period of highest risk for periventricular leukomalacia. We show that the clinically available anticonvulsant topiramate, when administered post-insult in vivo, is protective against selective hypoxic-ischemic white matter injury and decreases the subsequent neuromotor deficits. We further demonstrate that topiramate attenuates AMPA-kainate receptor-mediated cell death and calcium influx, as well as kainate-evoked currents in developing oligodendrocytes, similar to the AMPA-kainate receptor antagonist 6-nitro-7-sulfamoylbenzo-(f)quinoxaline-2,3-dione (NBQX). Notably, protective doses of NBQX and topiramate do not affect normal maturation and proliferation of oligodendrocytes either in vivo or in vitro. Taken together, these results suggest that AMPA-kainate receptor blockade may have potential for translation as a therapeutic strategy for periventricular leukomalacia and that the mechanism of protective efficacy of topiramate is caused at least in part by attenuation of excitotoxic injury to premyelinating oligodendrocytes in developing white matter.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Glutamate Receptor-Mediated Oligodendrocyte Toxicity in Periventricular Leukomalacia: A Protective Role for Topiramate

et al. 2004

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“…One hypothesis is that toxic interactions are mediated by activation of OL glutamate receptors (Tekkök and Goldberg, 2001). OLs express functional glutamate receptors (Gallo et al, 1994) and are injured in vitro via AMPA/kainate receptor activation (Yoshioka et al, 1995;McDonald et al, 1998;Fern and Moller, 2000;. AMPA/kainate receptor antagonists have been shown to reduce OL loss in ischemic WM (Tekkök and Goldberg, 2001).…”

Section: Introductionmentioning

confidence: 99%

White Matter Axon Vulnerability to AMPA/Kainate Receptor-Mediated Ischemic Injury Is Developmentally Regulated

McCarran¹,

Goldberg²

2007

J. Neurosci.

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Periventricular white matter injury (PWMI) is the leading cause of neurodevelopmental morbidity in survivors of premature birth.Cerebral ischemia is considered a major etiologic factor in the generation of PWMI. In adult white matter (WM), ischemic axonal damage is mediated by AMPA/kainate receptors. Mechanisms of ischemic axonal injury during development are not well defined. We used a murine brain slice model to characterize mechanisms of ischemic axonal injury in developing WM. Acute coronal brain slices were prepared from thy1-yellow fluorescent protein (

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“…The latter have been characterized most comprehensively in O-2A glial progenitor cells, which are endowed with voltage-and ligandactivated ion channels (Bevan et al, 1987;Barres et al, 1990a,b;Sakatani et al, 1992;Gallo et al, 1994). On commitment to either astrocyte or oligodendrocyte lineage, their ion channel complement changes markedly (Sontheimer et al, 1989;Barres et al, 1990b).…”

mentioning

confidence: 99%

Electrophysiological Changes That Accompany Reactive GliosisIn Vitro

1997

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An in vitro injury model was used to examine the electrophysiological changes that accompany reactive gliosis. Mechanical scarring of confluent spinal cord astrocytes led to a threefold increase in the proliferation of scar-associated astrocytes, as judged by bromodeoxyuridine (BrdU) labeling. Whole-cell patch-clamp recordings demonstrated that current profiles differed absolutely between nonproliferating (BrdU Ϫ ) and proliferating (BrdU ϩ ) astrocytes. The predominant current type expressed in BrdU Ϫ cells was an inwardly rectifying K ϩ current (K IR ; 1.3 pS/pF). BrdU Ϫ cells also expressed transient outward K ϩ currents, accounting for less than one-third of total K ϩ conductance (G). In contrast, proliferating BrdU ϩ astrocytes exhibited a dramatic, approximately threefold reduction in K IR (0.45 pS/pF) but showed a twofold increase in the conductance of both transient (K A ) (0.67-1.32 pS/pF) and sustained (K D ) (0.42-1.10 pS/pF) outwardly rectifying K ϩ currents, with a G KIR : G KD ratio of 0.4. Relative expression of G KIR :G KD led to more negative resting potentials in nonproliferating (Ϫ60 mV) versus proliferating astrocytes (Ϫ53 mV; p ϭ 0.015). Although 45% of the nonproliferating astrocytes expressed Na ϩ currents (0.47 pS/pF), the majority of proliferating cells expressed prominent Na ϩ currents (0.94 pS/pF). Injury-induced electrophysiological changes are rapid and transient, appearing within 4 hr postinjury and, with the exception of K IR , returning to control conductances within 24 hr. These differences between proliferating and nonproliferating astrocytes are reminiscent of electrophysiological changes observed during gliogenesis, suggesting that astrocytes undergoing secondary, injury-induced proliferation recapitulate the properties of immature glial cells. The switch in predominance from K IR to K D appears to be essential for proliferation and scar repair, because both processes were inhibited by blockade of K D .

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Excitatory amino acid receptors in glial progenitor cells: Molecular and functional properties

Cited by 98 publications

References 50 publications

Glutamate Receptor-Mediated Oligodendrocyte Toxicity in Periventricular Leukomalacia: A Protective Role for Topiramate

Glutamate Receptor-Mediated Oligodendrocyte Toxicity in Periventricular Leukomalacia: A Protective Role for Topiramate

White Matter Axon Vulnerability to AMPA/Kainate Receptor-Mediated Ischemic Injury Is Developmentally Regulated

Electrophysiological Changes That Accompany Reactive GliosisIn Vitro

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