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. Author manuscript; available in PMC: 2008 Jul 1.
Published in final edited form as: J Cereb Blood Flow Metab. 2007 Jan 10;27(7):1339–1351. doi: 10.1038/sj.jcbfm.9600440

Figure 7.

Figure 7

(A) Effects of pretreatment with SCH23390 or sulpiride on Na+,K+-ATPase activity in putamen of sham or hypoxia–ischemia (H–I) piglets at 3 h of recovery (n = 4 to 7 per group). (B) Representative Western blots of Na+,K+-ATPase (NKA) subunits α1 and α3 and phosphorylation of the combined α subunits at Ser943 and Ser23 in lysates from piglet putamen 3 h after hypoxia–ischemia (H–I). In total, 20 μg of protein was loaded onto gels, and antibodies against NKA α1 and α3 (1:50,000) and phosphorylated NKA at Ser943 and Ser23 (1:2000) were used to detect the protein at 110 kDa. Synaptophysin was used as a loading control. Lane 2 was treated for 4 h with 400 U/mL λ-phosphatase (λ-PPase). Bar graphs (means±s.d.) summarize the expression of NKA α1 (C) and α3 (D) subunits and phosphorylated NKA at Ser943 (E) and Ser23 (F), normalized to the sham + saline value, from four independent gels. *P < 0.05 versus sham groups treated with saline; #P < 0.05 versus H–I group treated with saline; one-way ANOVA followed by the Student–Newman–Keuls test.