Acute Brain Injury, NMDA Receptors, and Hydrogen Ions: Observations in Cortical Cell Cultures
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.
KeywordsNMDA Receptor Neuronal Injury NMDA Antagonist Glucose Deprivation Acute Brain Injury
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