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Bi, Mian; Gladbach, Amadeus; van Eersel, Janet; Ittner, Arne; Przybyla, Magdalena; van Hummel, Annika; Chua, Sook Wern; van der Hoven, Julia; Lee, Wei S; Müller, Julius; Parmar, Jasneet; Jonquieres, Georg von; Stefen, Holly; Guccione, Ernesto; Fath, Thomas; Housley, Gary D; Klugmann, Matthias; Ke, Yazi D; Ittner, Lars M
Nature communications, 09/2017, Letnik: 8, Številka: 1Journal Article
Neuronal excitotoxicity induced by aberrant excitation of glutamatergic receptors contributes to brain damage in stroke. Here we show that tau-deficient (tau ) mice are profoundly protected from excitotoxic brain damage and neurological deficits following experimental stroke, using a middle cerebral artery occlusion with reperfusion model. Mechanistically, we show that this protection is due to site-specific inhibition of glutamate-induced and Ras/ERK-mediated toxicity by accumulation of Ras-inhibiting SynGAP1, which resides in a post-synaptic complex with tau. Accordingly, reducing SynGAP1 levels in tau mice abolished the protection from pharmacologically induced excitotoxicity and middle cerebral artery occlusion-induced brain damage. Conversely, over-expression of SynGAP1 prevented excitotoxic ERK activation in wild-type neurons. Our findings suggest that tau mediates excitotoxic Ras/ERK signaling by controlling post-synaptic compartmentalization of SynGAP1.Excitotoxicity contributes to neuronal injury following stroke. Here the authors show that tau promotes excitotoxicity by a post-synaptic mechanism, involving site-specific control of ERK activation, in a mouse model of stroke.
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in: SICRIS
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