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Neurosci Lett. 2019 Mar 16;695:71-75. doi: 10.1016/j.neulet.2017.09.004. Epub 2017 Sep 5.

Pannexin-1 channels in epilepsy.

Author information

1
IBBME, University of Toronto, Rosebrugh Building, Room 407, 164 College St, Toronto, ON, M5S 3G9, Canada; Krembil Research Institute, University Health Network, 135 Nassau St, Toronto, ON, M5T 1M8, Canada. Electronic address: mark.aquilino@mail.utoronto.ca.
2
York University, 4700 Keele St, Toronto, ON, M3J 1P3, Canada.
3
York University, 4700 Keele St, Toronto, ON, M3J 1P3, Canada; Krembil Research Institute, University Health Network, 135 Nassau St, Toronto, ON, M5T 1M8, Canada.
4
IBBME, University of Toronto, Rosebrugh Building, Room 407, 164 College St, Toronto, ON, M5S 3G9, Canada; Krembil Research Institute, University Health Network, 135 Nassau St, Toronto, ON, M5T 1M8, Canada.

Abstract

Pannexin-1 (Panx1) expression is raised in several animal seizure models and in resected human epileptic brain tissue, suggesting relevance to epilepsy. Multiple factors that are characteristic of seizures are thought to regulate Panx1 channel opening, including elevated levels of extracellular K+. Panx1, when open, 1) releases ATP, glutamate, and other metabolites into the extracellular medium, and 2) may depolarize the membrane due to a channel reversal potential around 0mV. Resultant ATP release from stimulated Panx1 can activate purinergic receptors, including P2X7 receptors. Glutamate and other signaling molecules released by Panx1 opening may have both excitatory and inhibitory actions on seizure generation. This review examines the critical and complex roles of Panx1 channels in epilepsy, which could provide a basis for future therapeutics.

KEYWORDS:

ATP; Epilepsy; Glutamate; Pannexin; Potassium; Seizure

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