Figure 2

Increases in blood vessel density in rats vulnerable to stress. (a) Representative images of VWF immunohistochemistry. (b) VWF labeling was increased in the vHPC of SL/vulnerable rats relative to LL/resilient rats (n=6–7 per group; F2,3=6.02, P=0.006). There was no difference in the SL/vulnerable nor LL/resilient rats relative to the controls. (c) Representative western blot images of endothelial GluT1, which was (d) increased in the vHPC of SL/vulnerable rats relative to LL/resilient rats (n=6–7 per group; F2,17=5.65, P=0.013); there was no difference in GluT1 expression between SL/vulnerable nor LL/resilient rats relative to control rats. The astrocytic GluT1 was not altered. (e) Fifty micrometers confocal z-stacks of FITC-labeled blood vessels. (f) There was a negative correlation between latency to social defeat and average number of FITC-labeled vessels in the vHPC (n=15, r=−0.54, P=0.03). (g) There was not a significant correlation between latency to social defeat and the average number of FITC-labeled vessels in the dHPC (n=15). Data represent mean+s.e.m. *P<0.05. FITC, fluorescein isothiocyanate; LL, long latency; SL, short latency; vHPC, ventral hippocampus; VWF, von Willebrand Factor.