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Acute Brain Injury, NMDA Receptors, and Hydrogen Ions: Observations in Cortical Cell Cultures

  • Dennis W. Choi
  • Hannelore Monyer
  • Rona G. Giffard
  • Mark P. Goldberg
  • Chadwick W. Christine
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 268)

Abstract

Excess stimulation of NMDA receptors by endogenous glutamate likely contributes to the neuronal cell loss associated with several types of acute brain injury in vivo (Meldrum, 1985; Rothman and Olney, 1987, Choi, 1988), including ischemia (Simon et al., 1984), hypoglycemia (Wieloch, 1985), epilepsy (Labuyere et al., 1986) and trauma (Faden and Simon, 1988). Among the experiments supporting this statement are those studying the controlled delivery of insults to dispersed neuronal and glial cells in primary culture. Demonstration that a given pharmacological manipulation is neuroprotective in such cultures establishes that a beneficial effect can be produced directly on brain parenchyma, without involvement of systemic metabolism or alterations in blood flow. While organizational features of the intact nervous system are not expressed in cell culture, many intrinsic aspects of neuronal and glial cell behavior do appear to be qualitatively preserved. In particular, basic mechanisms relevant to glutamate transmission and glutamate neurotoxicity are present in cultured brain cells.

Keywords

NMDA Receptor Neuronal Injury NMDA Antagonist Glucose Deprivation Acute Brain Injury 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1990

Authors and Affiliations

  • Dennis W. Choi
    • 1
  • Hannelore Monyer
    • 1
  • Rona G. Giffard
    • 2
  • Mark P. Goldberg
    • 1
  • Chadwick W. Christine
    • 1
  1. 1.Department of NeurologyStanford University Medical CenterStanfordUSA
  2. 2.Department of AnesthesiaStanford University Medical CenterStanfordUSA

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