Fig. 5. SUR1-TRPM4 plays a critical role in brain swelling independent of infarct size.

(A) Proposed model of the functional axis comprised of SUR1-TRPM4, NCX1, and AQP4, with emphasis on SUR1-TRPM4. (B) Images of TTC-stained coronal brain sections following MCAO/R in a mouse with deletion of Abcc8/SUR1 in astrocytes (Ast-SUR1^KO) and a littermate control (Ast-SUR1^WT). Scale bar: 1 mm. Ischemia was induced by MCAO for 2 hours followed by reperfusion for 24 hours. Images are representative of 14 mice per group. (C and D) In mice as described in (B) with infarct volumes >40 mm³, ipsilateral hemispheric swelling following MCAO/R was quantified in slices from (C) WT mice administered vehicle (VEH) or glibenclamide (GLIB) at reperfusion and mice with constitutive or conditional astrocyte-specific deletion of Abcc8/SUR1 (Ast-SUR1^KO, Ast-SUR1^ERT2/KO) and littermate controls (Ast-SUR1^WT and Ast-SUR1^ERT2/WT), and (D) in slices from mice with global deletion of the gene encoding KIR6.2 or TRPM4 (KIR6.2^KO, TRPM4^KO) and littermate controls of the latter (TRPM4^WT [WT]). KIR6.2^WT littermates were not studied. Data are mean ± S.E. from N = 5 to 14 mice per group. **P<0.01 by ANOVA.