Excitotoxic mechanisms of ischemic injury in myelinated white matter (Q48273500)

10 February 2018

title

Excitotoxic mechanisms of ischemic injury in myelinated white matter (English)

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10 February 2018

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author name string

Selva Baltan Tekkök

series ordinal

1

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10 February 2018

ZuCheng Ye

series ordinal

2

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10 February 2018

publication date

14 February 2007

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10 February 2018

Journal of Cerebral Blood Flow & Metabolism

published in

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10 February 2018

volume

27

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issue

9

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10 February 2018

page(s)

1540-1552

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10 February 2018

Role of NMDA and non-NMDA ionotropic glutamate receptors in traumatic spinal cord axonal injury

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Ca(2+) influx through AMPA or kainate receptors alone is sufficient to initiate excitotoxicity in cultured oligodendrocytes.

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Metabolic substrates other than glucose support axon function in central white matter

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AMPA receptor activation is rapidly toxic to cortical astrocytes when desensitization is blocked.

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Voltage-gated calcium channels in CNS white matter: role in anoxic injury

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NBQX attenuates excitotoxic injury in developing white matter

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Excitatory amino acid receptors in glia: different subtypes for distinct functions?

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Expression and regulation of a glutamate receptor subunit by bFGF in oligodendrocyte progenitors

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Mechanisms of ischaemic damage to central white matter axons: a quantitative histological analysis using rat optic nerve

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New light on white matter

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Subcellular heterogeneity of voltage-gated Ca2+ channels in cells of the oligodendrocyte lineage

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Important role of reverse Na(+)-Ca(2+) exchange in spinal cord white matter injury at physiological temperature

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Novel injury mechanism in anoxia and trauma of spinal cord white matter: glutamate release via reverse Na+-dependent glutamate transport.

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Mechanisms of ionotropic glutamate receptor-mediated excitotoxicity in isolated spinal cord white matter

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Na(+)-K(+)-ATPase inhibition and depolarization induce glutamate release via reverse Na(+)-dependent transport in spinal cord white matter

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Glutamate receptor-mediated toxicity in optic nerve oligodendrocytes.

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Characteristics of acute and chronic kainate excitotoxic damage to the optic nerve

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Oligodendrocytes from forebrain are highly vulnerable to AMPA/kainate receptor-mediated excitotoxicity

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NMDA receptors mediate calcium accumulation in myelin during chemical ischaemia

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Depolarization-induced Ca2+ release in ischemic spinal cord white matter involves L-type Ca2+ channel activation of ryanodine receptors

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Anoxic injury of CNS white matter: protective effect of ketamine.

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Mechanisms of H+ and Na+ changes induced by glutamate, kainate, and D-aspartate in rat hippocampal astrocytes.

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NMDA receptors are expressed in developing oligodendrocyte processes and mediate injury

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AMPA and kainate receptors each mediate excitotoxicity in oligodendroglial cultures

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Mechanisms of 1S,3R-ACPD-induced neuroprotection in rat hippocampal slices subjected to oxygen and glucose deprivation

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7 January 2021

Role of extracellular calcium in anoxic injury of mammalian central white matter

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7 January 2021

Ionic mechanisms of anoxic injury in mammalian CNS white matter: role of Na+ channels and Na(+)-Ca2+ exchanger.

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White matter injury mechanisms

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Anoxia effects on CNS function and survival: regional differences

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Axon function persists during anoxia in mammalian white matter

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7 January 2021

Ampa/kainate receptor activation mediates hypoxic oligodendrocyte death and axonal injury in cerebral white matter.

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7 January 2021

Traumatic axonal injury induces calcium influx modulated by tetrodotoxin-sensitive sodium channels

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7 January 2021

Evidence that local non-NMDA receptors contribute to functional deficits in contusive spinal cord injury

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7 January 2021

Amelioration of functional deficits from spinal cord trauma with systemically administered NBQX, an antagonist of non-N-methyl-D-aspartate receptors

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7 January 2021

NMDA receptor blockade fails to alter axonal injury in focal cerebral ischemia

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7 January 2021

Functional hemichannels in astrocytes: a novel mechanism of glutamate release.

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7 January 2021

Identifiers

DOI

10.1038/SJ.JCBFM.9600455

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10 February 2018

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10 February 2018