Neuronal pannexin-1 channels are not molecular routes of water influx during spreading depolarization-induced dendritic beading
Autor: | Roger J. Thompson, Jeremy Sword, Sergei A. Kirov, Phil L Wang, Deborah Croom |
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Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
Aquaporin Mice Transgenic Nerve Tissue Proteins Connexins Neuronal swelling 03 medical and health sciences 0302 clinical medicine Animals Microscopy Confocal Chemistry Cytotoxic edema Cortical Spreading Depression Brain Water Biological Transport Depolarization Dendrites Pannexin Mice transgenic Cell biology Mefloquine Microscopy Fluorescence Multiphoton 030104 developmental biology Neurology Astrocytes Cortical spreading depression Neurology (clinical) Brief Communications Cardiology and Cardiovascular Medicine 030217 neurology & neurosurgery Water entry |
Zdroj: | Journal of Cerebral Blood Flow & Metabolism. 37:1626-1633 |
ISSN: | 1559-7016 0271-678X |
Popis: | Spreading depolarization-induced focal dendritic swelling (beading) is an early hallmark of neuronal cytotoxic edema. Pyramidal neurons lack membrane-bound aquaporins posing a question of how water enters neurons during spreading depolarization. Recently, we have identified chloride-coupled transport mechanisms that can, at least in part, participate in dendritic beading. Yet transporter-mediated ion and water fluxes could be paralleled by water entry through additional pathways such as large-pore pannexin-1 channels opened by spreading depolarization. Using real-time in vivo two-photon imaging in mice with pharmacological inhibition or conditional genetic deletion of pannexin-1, we showed that pannexin-1 channels are not required for spreading depolarization-induced focal dendritic swelling. |
Databáze: | OpenAIRE |
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