Increased seizure duration and slowed potassium kinetics in mice lacking aquaporin-4 water channels

✍ Scribed by Devin K. Binder; Xiaoming Yao; Zsolt Zador; Thomas J. Sick; Alan S. Verkman; Geoffrey T. Manley

• Book ID: 102225843
• Publisher: John Wiley and Sons
• Year: 2006
• Tongue: English
• Weight: 308 KB
• Volume: 53
• Category: Article
• ISSN: 0894-1491
• DOI: 10.1002/glia.20318

✦ Synopsis

Abstract

The glial water channel aquaporin‐4 (AQP4) has been hypothesized to modulate water and potassium fluxes associated with neuronal activity. In this study, we examined the seizure phenotype of AQP4 −/− mice using in vivo electrical stimulation and electroencephalographic (EEG) recording. AQP4 −/− mice were found to have dramatically prolonged stimulation‐evoked seizures after hippocampal stimulation compared to wild‐type controls (33 ± 2 s vs. 13 ± 2 s). In addition, AQP4 −/− mice were found to have a higher seizure threshold (167 ± 17 μA vs. 114 ± 10 μA). To assess a potential effect of AQP4 on potassium kinetics, we used in vivo recording with potassium‐sensitive microelectrodes after direct cortical stimulation. Although there was no significant difference in baseline or peak [K^+^]~o~, the rise time to peak [K^+^]~o~ (t~1/2~, 2.3 ± 0.5 s) as well as the recovery to baseline [K^+^]~o~ (t~1/2~, 15.6 ± 1.5 s) were slowed in AQP4 −/− mice compared to WT mice (t~1/2~, 0.5 ± 0.1 and 6.6 ± 0.7 s, respectively). These results implicate AQP4 in the expression and termination of seizure activity and support the hypothesis that AQP4 is coupled to potassium homeostasis in vivo. © 2006 Wiley‐Liss, Inc.