Glucose deprivation neuronal injury in cortical culture

Hannelore Monyer, Mark P. Goldberg, Dennis W. Choi

Research output: Contribution to journalArticle

79 Scopus citations

Abstract

Murine cortical cell cultures deprived of glucose for 6-8 h developed extensive neuronal degeneration, apparent both morphologically and by efflux of lactate dehydrogenase to the bathing medium. This neuronal damage could be substantially reduced by addition of d-2-amino-5-phosphonovalerate (d-APV), in a concentration-dependent (IC50 about 2 μM) and stereospecific (d-APV more potent than l-APV) fashion. A similar neuron-protective effect could also be obtained with several other NMDA antagonists, 2-amino-7-phosphonoheptanoate, phencyclidine, MK-801, ketamine, and (+)-SKF 10,047, as well as with the broad spectrum glutamate antagonist kynurenate. In contrast, little protection could be obtained with γ-d-glutamylaminomethyl sulfonate and l-glutamate diethyl ester, compounds which have been reported to act primarily at non-NMDA receptors. These observations support the hypothesis that glucose deprivation-induced cortical neuronal injury is largely mediated by NMDA receptors, and suggest that cell culture methodology can be useful in the quantitative characterization of that injury.

Original languageEnglish (US)
Pages (from-to)347-354
Number of pages8
JournalBrain Research
Volume483
Issue number2
DOIs
StatePublished - Apr 3 1989

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Keywords

  • Asparatate
  • Cell culture
  • Cortex
  • Excitatory amino acid
  • Glutamate
  • N-Methyl-d-aspartate receptor
  • Neurotoxicity

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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