Neuronal pannexin-1 channels are not molecular routes of water influx during spreading depolarization-induced dendritic beading

Jeremy Sword, Deborah Croom, Phil L. Wang, Roger J. Thompson, Sergei A. Kirov

Research output: Contribution to journalArticle

8 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)1626-1633
Number of pages8
JournalJournal of Cerebral Blood Flow and Metabolism
Volume37
Issue number5
DOIs
StatePublished - May 1 2017

Keywords

  • Conditional pannexin-1 knock-out
  • mefloquine
  • neuronal swelling
  • two-photon imaging
  • viral vectors

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine

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