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

作者: Dennis W. Choi , Hannelore Monyer , Rona G. Giffard , Mark P. Goldberg , Chadwick W. Christine

DOI: 10.1007/978-1-4684-5769-8_55

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

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