Title |
Ischemia-induced cell depolarization: does the hyperpolarization-activated cation channel HCN2 affect the outcome after stroke in mice?
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Published in |
Experimental & Translational Stroke Medicine, December 2013
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DOI | 10.1186/2040-7378-5-16 |
Pubmed ID | |
Authors |
Petra Ehling, Eva Göb, Stefan Bittner, Thomas Budde, Andreas Ludwig, Christoph Kleinschnitz, Sven G Meuth |
Abstract |
Brain ischemia is known to include neuronal cell death and persisting neurological deficits. A lack of oxygen and glucose are considered to be key mediators of ischemic neurodegeneration while the exact mechanisms are yet unclear. In former studies the expression of two different two-pore domain potassium (K2P) channels (TASK1, TREK1) were shown to ameliorate neuronal damage due to cerebral ischemia. In neurons, TASK channels carrying hyperpolarizing K+ leak currents, and the pacemaker channel HCN2, carrying depolarizing Ih, stabilize the membrane potential by a mutual functional interaction. It is assumed that this ionic interplay between TASK and HCN2 channels enhances the resistance of neurons to insults accompanied by extracellular pH shifts. |
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