| First Author | Strohschein S | Year | 2011 |
| Journal | Glia | Volume | 59 |
| Issue | 6 | Pages | 973-80 |
| PubMed ID | 21446052 | Mgi Jnum | J:171206 |
| Mgi Id | MGI:4948995 | Doi | 10.1002/glia.21169 |
| Citation | Strohschein S, et al. (2011) Impact of aquaporin-4 channels on K(+) buffering and gap junction coupling in the hippocampus. Glia 59(6):973-80 |
| abstractText | Aquaporin-4 (AQP4) is the main water channel in the brain and primarily localized to astrocytes where the channels are thought to contribute to water and K(+) homeostasis. The close apposition of AQP4 and inward rectifier K(+) 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(+) concentration ([K(+) ](o) ) in murine hippocampal slices. Recordings with K(+) -selective microelectrodes combined with field potential analyses were compared in wild type (wt) and AQP4 knockout (AQP4(-/-) ) 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(+) ](o) in the stratum pyramidale of AQP4(-/-) mice indicating reduced glial swelling and a larger extracellular space when compared with control tissue. Moreover, the data hintat an impairment of the glial Na(+) /K(+) ATPase in AQP4-deficient astrocytes. In a next step, we investigated the laminar profile of [K(+) ](o) by moving the recording electrode from the stratum pyramidale toward the hippocampal fissure. At distances beyond 300 mum from the pyramidal layer, the stimulation-induced, normalized increases of [K(+) ](o) in AQP4(-/-) mice exceeded the corresponding values of wt mice, indicating facilitated spatial buffering. Astrocytes in AQP4(-/-) mice also displayed enhanced tracer coupling, which might underlie the improved spatial re- distribution of [K(+) ](o) in the hippocampus. These findings highlight the role of AQP4 channels in the regulation of K(+) homeostasis. (c) 2011 Wiley-Liss, Inc. |
