Hypoxia/reoxygenation induces cell injury via different mechanisms in cultured rat cortical neurons and glial cells

Ju Yu Wang, Andrew Y C Shum, Jia Yi Wang

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Hypoxia/reoxygenation (H/R) causes cell injury/death. We examined the protection by drugs intervening at various stages of the injury cascade in cultured neurons and glia. Primary cultures of rat cortical neurons and mixed glia were subjected to H/R. Measurements of cell death (by lactate dehydrogenase release into the medium) and viability (by MTT reduction) indicated that H/R led to time-dependent injury in both neuronal and mixed glial cultures. The extent of cell injury in neurons was significantly greater than in glia cells. Pretreatment with (+)-MK-801 hydrogen maleate (MK-801) (an N-methyl-D-aspartate antagonist), Nω-nitro-L-arginine methyl ester (L-NAME) (an inhibitor of nitric oxide synthase) or free radical scavengers reduced the extent of the H/R-elicited neuronal damage. MK-801, in contrast, was without effect on glial cells while L-NAME was effective. Our results suggest differential mechanism(s) and susceptibility to injury caused by H/R for neurons and mixed glia.

Original languageEnglish
Pages (from-to)187-191
Number of pages5
JournalNeuroscience Letters
Volume322
Issue number3
Publication statusPublished - Apr 12 2002
Externally publishedYes

Fingerprint

Neuroglia
Neurons
Dizocilpine Maleate
Wounds and Injuries
NG-Nitroarginine Methyl Ester
Cell Death
Free Radical Scavengers
N-Methylaspartate
L-Lactate Dehydrogenase
Nitric Oxide Synthase
Hypoxia
Pharmaceutical Preparations

Keywords

  • Cell injury
  • Cortical culture
  • Free radicals
  • Hypoxia/reoxygenation
  • N-methyl-D-aspartate receptor
  • Nitric oxide

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Hypoxia/reoxygenation induces cell injury via different mechanisms in cultured rat cortical neurons and glial cells. / Wang, Ju Yu; Shum, Andrew Y C; Wang, Jia Yi.

In: Neuroscience Letters, Vol. 322, No. 3, 12.04.2002, p. 187-191.

Research output: Contribution to journalArticle

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