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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 6. Effect of GluN2A-NMDAR inhibition on ischemia-induced normal gait impairment, motor coordination and sensorimotor deficit in hyperhomocysteinemic rats.

Figure 6.

(A-G) Control, hyperhomocysteinemic (HHcy) and hyperhomocysteinemic rats treated with GluN2A-NMDAR inhibitor NVP-AAM077 (HHcy + NVP) were subjected to MCAO followed by reperfusion. Quantitative analysis of (A) Maximum contact area (mm2); (B) Print area (mm2) and (C) Print position (cm) in the affected forepaw (contralateral) assessed by CatWalk 7 days after MCAO (control: n = 11, HHcy: n = 14, HHcy + NVP: n = 11). Quantitative analysis of (D) spontaneous contralateral forelimb use assessed using cylinder test (day 8 post MCAO; control: n = 7, HHcy: n = 14, HHcy + NVP: n = 11); (E) motor impairment and balance assessed using the rotarod test (day 8 post MCAO; control: n = 12, HHcy: n = 14, HHcy + NVP: n = 11); (F, G) mean latency to detect (F) and remove (G) an adhesive label from the contralateral forepaw (time in seconds) assessed as a measure of sensorimotor function (day 9 post MCAO; control: n = 12, HHcy: n = 15, HHcy + NVP: n = 11). All data are expressed as mean ± SEM; *p < 0.05 and **p < 0.001 for control vs. HHcy rats; and #p < 0.05 and ##p < 0.001 for HHcy vs. HHcy + NVP treated rats.