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Intracellular pH reduction prevents excitotoxic and ischemic neuronal death by inhibiting NADPH oxidase

Lam, Tina I., Brennan-Minnella, Angela M., Won, Seok Joon, Shen, Yiguo, Hefner, Colleen, Shi, Yejie, Sun, Dandan, Swanson, Raymond A.·2013·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.1313029110
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Abstract

Significance: Activation of NMDA-type glutamate receptors produces neuronal excitotoxicity, a primary cause of cell death in stroke and other neurological disorders. This cell death process requires superoxide release by neuronal NADPH oxidase. Results presented here show that small reductions in intracellular pH uncouple neuronal NADPH oxidase from NMDA receptor activation, and thereby prevent neuronal death. The findings establish a link between metabolic activity and excitotoxicity, and identify a mechanism by which mild acidosis improves outcome after excitotoxic and ischemic brain insults. The findings also suggest that variations in intracellular pH associated with physiological brain activity may likewise influence the cell-to-cell signaling normally mediated by neuronal superoxide release.

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  • Arteriovenous gradients demonstrated consistent consumption of glucose and oxygen as brains reached normothermia, with concurrent CO2 production and a physiological drop in pH.

    “Arteriovenous gradients demonstrated consistent consumption of glucose and oxygen as the brains reached normothermia, with a concurrent production in CO2 and a physiological drop in pH39.”

    From Restoration of brain circulation and cellular functions hours post-mortem (2019) · cites this paper as [39]

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Metadata

Authors
Lam, T. I., Brennan-Minnella, A. M., Won, S. J., Shen, Y., Hefner, C., Shi, Y., Sun, D., & Swanson, R. A.
Affiliations
  • Department of Neurology, University of California, San Francisco, CA 94121;
  • Department of Neurology, University of Pittsburgh, Pittsburgh, PA 15213
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
2013-10-25
Volume
110
Issue
46
ISSN
  • 0027-8424
  • 1091-6490
DOI
10.1073/pnas.1313029110
Cited by
79
References
0
Language
en

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