Neuronal pannexin-1 channels are not molecular routes of water influx during spreading depolarization-induced dendritic beading. Issue 5 (May 2017)

• Record Type: Journal Article
• Authors: Sword, Jeremy; Croom, Deborah; Wang, Phil L; Thompson, Roger J; Kirov, Sergei A
• Is Part Of: Journal of cerebral blood flow & metabolism. Volume 37:Issue 5(2017)
• Page Start: 1626
• Page End: 1633
• Publication Date: 2017-05
• Subjects: Conditional pannexin-1 knock-out -- mefloquine -- neuronal swelling -- two-photon imaging -- viral vectors; Cerebral circulation -- Periodicals; Brain -- Metabolism -- Periodicals; Brain -- Blood-vessels -- Periodicals; Cerebrovascular disease -- Periodicals; 612.824
• DOI: 10.1177/0271678X16639328
• Languages: English
• ISSNs: 0271-678X

Abstract

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.