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Acidotoxicity Trumps Excitotoxicity in Ischemic Brain
Roger P. Simon, MD
Arch Neurol. 2006;63:1368-1371.
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INTRODUCTION
Plum entitled his 1982 Wartenberg Lecture "What Causes Infarction in Ischemic Brain?"1 This question remains incompletely answered 2 decades later, during which excitatory amino acids and calcium toxicity have been central research and therapeutic targets. Recently, attention has returned to a central neurochemical feature of ischemic brain injury, acidosis, which was focused on in Plum's lecture. Targeting this effector of injury as therapy for brain ischemia now may be closer at hand and may result in robust neuroprotection.
MORPHOLOGY OFFERS CLUES TO ISCHEMIA PATHOGENESIS
In the 1970s, Brown and Brierley2 described the prodromal morphologic features of ischemic cell change as that of microvacuolization in selectively vulnerable neurons (Figure 1). In 1984, Brian Meldrum and I,3 working at the Institute of Psychiatry in London, England, looked again at these vacuoles. We used ultrastructural studies of ischemic brain treated with the then new oxalate-pyroantimonate technique, with which calcium could be visualized as . . . [Full Text of this Article]
EXPERIMENTAL EPILEPSY SUGGESTS THERAPY FOR ISCHEMIA
FAILURE OF CLINICAL TRIALS
ACID-SENSING ION CHANNELS IN THE BRAIN
ACIDOTOXICITY
BLOCKADE OF ASICS AS A NEW THERAPY FOR STROKE
CODA
CONCLUSIONS
AUTHOR INFORMATION
Author Affiliation: Legacy Research, Robert S. Dow Neurobiology Laboratories, Portland, Ore.
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Murphy et al.
J. Neurosci. 2008;28:1756-1772.
ABSTRACT
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