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. Author manuscript; available in PMC: 2022 May 1.
Published in final edited form as: J Neurochem. 2020 Oct 6;157(4):1366–1376. doi: 10.1111/jnc.15195

Figure 2.

Figure 2.

Delayed deletion of neuronal Rac1 led to poorer functional recovery after ischemic stroke in mice. Tamoxifen (2 mg/40 g/daily) was intraperitoneally injected to Thy1-creER/Rac1-floxed (T-Rac1-floxed) mice from day 7 to day 11 after stroke. Same process was performed on Rac1-floxed mice as control. (A) Immunohistochemistry assessment of cerebral Rac1 expression (red, Alexa Fluor 647) on neurons (NeuN, green, Alexa Fluor 594) 28 days after stroke (N = 4/each group). Arrows indicated the Rac1 positive neurons (yellow). Functional recovery assessed by (B) novel object recognition test, (C) adhesive removal test and (D) pellet reaching test before (Pre) up to 28 days after stroke (N = 7 in the Rac1-floxed group, N = 8 in the T-Rac1-floxed group). N = number of animals. *p < 0.05, ***p < 0.001. Mann-Whitney test was used for immune-staining. Two-way ANOVA with subsequent Bonferonni test was applied for behavioral tests.