Matthias Endres, Klaus Fink, Jinmin Zhu, Nancy E. Stagliano, Vimala Bondada, James W. Geddes, Toshifumi Azuma, Mark P. Mattson, David J. Kwiatkowski, Michael A. Moskowitz
J Clin Invest.
1999;
103(3):347–354
doi:10.1172/JCI4953
This article Copyright © 1999, The American Society for Clinical Investigation
Abstract
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ncreased Ca2+ influx through activated N-methyl-D-aspartate (NMDA) receptors and voltage-dependent Ca2+ channels (VDCC) is a major determinant of cell injury following brain ischemia. The activity of these channels is modulated by dynamic changes in the actin cytoskeleton, which may occur, in part, through the actions of the actin filament–severing protein gelsolin. We show that gelsolin-null neurons have enhanced cell death and rapid, sustained elevation of Ca2+ levels following glucose/oxygen deprivation, as well as augmented cytosolic Ca2+ levels in nerve terminals following depolarization in vitro. Moreover, major increases in infarct size are seen in gelsolin-null mice after reversible middle cerebral artery occlusion, compared with controls. In addition, treatment with cytochalasin D, a fungal toxin that depolymerizes actin filaments, reduced the infarct size of both gelsolin-null and control mice to the same final volume. Hence, enhancement or mimicry of gelsolin activity may be neuroprotective during stroke.
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