Impact of aquaporin-4 channels on K+ buffering and gap junction coupling in the hippocampus
✍ Scribed by Susan Strohschein; Kerstin Hüttmann; Siegrun Gabriel; Devin K. Binder; Uwe Heinemann; Christian Steinhäuser
- Publisher
- John Wiley and Sons
- Year
- 2011
- Tongue
- English
- Weight
- 305 KB
- Volume
- 59
- Category
- Article
- ISSN
- 0894-1491
No coin nor oath required. For personal study only.
✦ Synopsis
is the main water channel in the brain and primarily localized to astrocytes where the channels are thought to contribute to water and K 1 homeostasis. The close apposition of AQP4 and inward rectifier K 1 channels (Kir4.1) led to the hypothesis of direct functional interactions between both channels. We investigated the impact of AQP4 on stimulus-induced alterations of the extracellular K 1 concentration ([K 1 ] o ) in murine hippocampal slices. Recordings with K 1 -selective microelectrodes combined with field potential analyses were compared in wild type (wt) and AQP4 knockout (AQP4 2/2 ) mice. Astrocyte gap junction coupling was assessed with tracer filling during patch clamp recording. Antidromic fiber stimulation in the alveus evoked smaller increases and slower recovery of [K 1 ] o in the stratum pyramidale of AQP4 2/2 mice indicating reduced glial swelling and a larger extracellular space when compared with control tissue. Moreover, the data hint at an impairment of the glial Na 1 /K 1 ATPase in AQP4-deficient astrocytes. In a next step, we investigated the laminar profile of [K 1 ] o by moving the recording electrode from the stratum pyramidale toward the hippocampal fissure. At distances beyond 300 lm from the pyramidal layer, the stimulation-induced, normalized increases of [K 1 ] o in AQP4 2/2 mice exceeded the corresponding values of wt mice, indicating facilitated spatial buffering. Astrocytes in AQP4 2/2 mice also displayed enhanced tracer coupling, which might underlie the improved spatial redistribution of [K 1 ] o in the hippocampus. These findings highlight the role of AQP4 channels in the regulation of K 1 homeostasis. V