Fig. 2.

Egr1-/- mice showed less brain damage following transient MCAO compared to Egr1+/+ littermates. Panel a shows 2,3,5-triphenyl tetrazolium chloride-stained serial brain sections of representative mice of Egr1+/+ and Egr1-/- genotype. Panel b shows the infarct volumes and panel c shows the neurological scores in the Egr1-/- and Egr1+/+ mice subjected to transient MCAO and 3 days of reperfusion. The values in B are mean ± SD (n = 11 and 13 for Egr1+/+ and Egr1-/- cohorts). A 5-point neurological scale was used in which a score of 0 suggests no neurological deficit (normal), 1 suggests mild neurological deficit (failure to extend right forepaw fully), 2 suggests moderate neurological deficit (circling to the right), 3 suggests severe neurological deficit (falling to the right), and 4 suggests very severe neurological deficit (the animal could not walk spontaneously; depressed level of consciousness). No mice entered grade 4. Neuroscores for the 2 Egr1+/+ mice that died between day 1 and 3 of reperfusion were not shown on day 3. In panels b and c, *p < 0.05 compared to Egr1+/+ mice by one-way ANOVA followed by Tukey-Kramer multiple comparisons post-test. The rCBF (mean ± SD; n = 13/group) measured by laser-Doppler during MCAO and reperfusion was not significantly different between the 2 genotypes (d). Panel e shows the tail DNA genotyping of representative mice from the Egr1+/+ and Egr1-/- cohorts. As expected, the PCR products were observed to be ~400 bp for Egr1+/+ and ~420 bp for Egr1-/- mice (e). Following transient MCAO and 1 day reperfusion, the cerebral cortex of the Egr1+/+ mice showed Egr1 immunoreactive protein band which was not observed in case of Egr1-/- mice (f).