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The Journal of Neuroscience, August 15, 1998, 18(16):6290-6299

Extracellular Acidity Potentiates AMPA Receptor-Mediated Cortical Neuronal Death

John W. McDonald, Tim Bhattacharyya, Stefano L. Sensi, Doug Lobner, Howard S. Ying, Lorella M.T. Canzoniero, and Dennis W. Choi

Center for the Study of Nervous System Injury and Department of Neurology, Washington University School of Medicine, St. Louis, Missouri 63110

The extracellular acidity that accompanies brain hypoxia-ischemia is known to reduce both NMDA and AMPA-kainate receptor-mediated currents and NMDA receptor-mediated neurotoxicity. Although a protective effect of acidic pH on AMPA-kainate receptor-mediated excitotoxicity has been assumed, such has not been demonstrated. Paradoxically, we found that lowering extracellular pH selectively increased AMPA-kainate receptor-mediated neurotoxicity in neocortical cell cultures, despite reducing peak elevations in intracellular free Ca2+. This injury potentiation may, at least in part, be related to a slowed recovery of intracellular Ca2+ homeostasis, observed after AMPA-kainate receptor activation, but not after NMDA receptor activation or exposure to high K+. The ability of acidic pH to selectively augment AMPA-kainate receptor-mediated excitotoxicity may contribute to the prominent role that these receptors play in selective neuronal death after transient global ischemia.

Key words: AMPA; murine neuronal culture; pH; excitotoxicity; cyclothiazide; acidosis

Copyright © 1998 Society for Neuroscience  0270-6474/98/18166290-10$05.00/0


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