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The Journal of Neuroscience, March 15, 2001, 21(6):2058-2066
Reduction of Potassium Currents and Phosphatidylinositol
3-Kinase-Dependent Akt Phosphorylation by Tumor
Necrosis Factor- Rescues Axotomized Retinal Ganglion Cells from
Retrograde Cell Death In Vivo
Ricarda
Diem,
Roman
Meyer,
Jochen H.
Weishaupt, and
Mathias
Bähr
Neurologische Universitätsklinik, 72076 Tübingen,
Germany
Tumor-necrosis-factor- (TNF-) prevented secondary death of
retinal ganglion cells (RGCs) after axotomy of the optic nerve in vivo. This RGC rescue was confirmed in
vitro in a mixed retinal culture model. In accordance with our
previous findings, TNF- decreased outward potassium currents in
RGCs. Antagonism of the TNF--induced decrease in outward potassium
currents with the potassium channel opener minoxidilsulfate (as
verified by electrophysiology) abolished neuroprotection. Western blot
analysis revealed an upregulation of phospho-Akt as a consequence of
TNF--induced potassium current reduction. Inhibition of the
phosphatidylinositol 3-kinase-Akt pathway with wortmannin decreased
TNF--promoted RGC survival. These data point to a functionally
relevant cytokine-dependent neuroprotective signaling cascade in adult
CNS neurons.
Key words:
tumor necrosis factor-; retinal ganglion cells; neuroprotection; outward potassium current; PKB/Akt; PI3-K; retrograde
cell death
Copyright © 2001 Society for Neuroscience 0270-6474/01/2162058-09$05.00/0
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