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. Author manuscript; available in PMC: 2016 Oct 1.
Published in final edited form as: Glia. 2015 May 6;63(10):1860–1869. doi: 10.1002/glia.22853

Figure 5.

Figure 5

Modeling predicts slower propagation of spreading depression in AQP4−/− mice. A. [K+]e changes during the initial phase of CSD were modelled as described by Zandt et al. (Zandt et al. 2013) using experimentally determined values for K+ release rate (AQP4+/+ 3.95 mM/s, AQP4−/− 1.72 mM/s), reuptake rate constant (AQP4+/+ 0.0226 s−1, AQP4−/− 0.0116 s−1) and effective diffusion coefficient (AQP4+/+ 0.796 × 10−5 cm2/s, AQP4−/− 0.907 × 10−5 cm2/s). Neuronal K+ release threshold was set at 10 mM (dotted line). B. Dependence of CSD propagation velocity on rates of K+ release rate and removal modelled for a neuronal release threshold of 10 mM K+ and effective K+ diffusion coefficient of 2 × 10−5 cm2/s. Dotted lines denote experimentally measured release and removal rates in AQP4+/+ and AQP4−/− mice. C. Dependence of relative CSD propagation velocity on K+ diffusion coefficient and the threshold for neuronal K+ release.