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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 5. Effect of GluN2A-NMDARs inhibition on the progression of ischemic brain damage in hyperhomocysteinemic rats.

Figure 5.

(A) Representative T2 maps from days 1, 3 and 14 after MCAO, acquired from hyperhomocysteinemic rats treated with vehicle (HHcy) or NVPAAM077 (HHcy + NVP), showing changes in ischemic lesion size from rostral to caudal regions of the brain. Corresponding bar diagram provide quantitative analysis of total infarct volume, expressed as mean ± SEM (on days 1 and 3 - HHcy: n = 15; on day 14 - HHcy: n = 14; on days 1, 3 and 14 - HHcy + NVP: n = 11). (B) Representative ADC maps acquired from HHcy and HHcy + NVP treated rats at day 14 post-MCAO, featuring hyperintense areas that co-loacalize with the lesion area in the T2 maps at day 14 post-MCAO. Quantitative analysis of ADC values in the lesion area, expressed as mean ± SEM (HHcy: n = 14, HHcy + NVP: n = 10). (C) Representative FA maps acquired from the same slices as ADC and T2 maps at 14 days post-MCAO as well as quantitative analysis of FA values expressed as mean ± SEM (HHcy: n = 14, HHcy + NVP: n = 10). *p < 0.01, **p < 0.005 and ***p < 0.001 for HHCy vs. HHcy + NVP treated rats.