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. Author manuscript; available in PMC: 2020 Jul 1.
Published in final edited form as: Neurobiol Dis. 2019 Mar 15;127:287–302. doi: 10.1016/j.nbd.2019.03.012

Figure 7. Effect of GluN2A-NMDAR gene deletion on the exacerbation of ischemic brain damage in hyperhomocysteinemic mice.

Figure 7.

(A) Schematic representation of the timeline of blood collection following implantation of osmotic pump, MCAO, reperfusion and MRI scan in wild-type (WT) and GluN2A-KO mice. (B) Quantitative analysis of total plasma homocysteine level in WT and hyperhomocysteinemic (HHcy) mice before (0 day) and after (3 and 5 days) implantation of pump. Values are expressed as mean ± SEM (n = 3–5 / group); (C) Representative photomicrographs of T2 maps acquired from control-WT, HHcy-WT, control-GluN2A-KO and HHcy-GluN2A-KO mice following MCAO (30 min) and reperfusion (24h). (D) Quantitative analysis of total infarct volume in WT (control and HHcy) and GluN2A-KO (control or HHcy) mice. Values are expressed as mean ± SEM (control-WT: n = 8, HHcy-WT: n = 5, control-GluN2A-KO: n = 3, HHcy-GluN2A-KO: n = 3). *p < 0.01 for WT mice day 0 vs. WT mice day 3 or 5; #p < 0.01 for GluN2A-KO mice day 0 vs. GluN2A-KO mice day 3 or 5. **p < 0.001 for control-WT vs. HHcy-WT mice.