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. 2012 Jul 22;4(3):302–315.

Figure 3.

Figure 3

HIV-1 Tat intracerebroventricular (ICV) injection promotes neuronal cell loss and Th1 associated microglial activation in CD45 deficient mice. (A) CD45 deficiency promoted HIV-1 Tat induced neuronal damage/death. Half-brain sections from 3-month-old CD45 sufficient and deficient mice (C57BL/6J, CD45-/-) after ICV injection of Tat (500 ng/mouse) or heat inactivate HIV-1 Tat (500 ng/mouse) as a control for 24 hr, were stained by NeuN antibody (a-d), and GFAP (i-l) antibody. Counter staining was performed by DAPI (e–h, m-p) (n=3 for each group). HIV-1 Tat treatment induced neuronal cell damage/loss in CD45 sufficient mice compared with PBS treated mice (b vs. a). Furthermore, HIV-1 Tat treatment in the CD45-/- mice further promoted neuronal death/damage (d vs. a-c). Further, astrocyte activation was shown highest in HIV-1 Tat treated mice compared to the CD45 deficient condition (l vs. i-k). Images are represented 10 × object magnifications. (B) Brain homogenates were prepared from half of brain tissues and probed by western blot using antibodies against Bcl-XL and Bax. In CD45-/- mice, the ratio of Bcl-XL to Bax trended to decrease but did not reach significance due to the relatively small number of animals. (C) TNF-α expression is significantly upregulated in the HIV-1 Tat ICV injected CD45-/- mice compared to heat-inactivated HIV-1 Tat injected mice (* p < 0.05, n=3 for each group).