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. Author manuscript; available in PMC: 2015 Jan 28.
Published in final edited form as: J Neurovirol. 2004 Jun;10(3):141–151. doi: 10.1080/13550280490441103

Figure 3.

Figure 3

HIV-1 Tat1-72 and gp120 reduced striatal neuron survival at 24, 48, and 72 hours in vitro. Both Tat (100 nM) (A) and gp120 (500 pM) (B) significantly increased the proportion of dying neurons at 48 and/or 72 h (*P < 0.05 versus vehicle-treated controls). The cytotoxic effects of gp120, but not Tat1-72, were significantly attenuated by the caspase inhibitor Z-DEVD-FMK (30 µM; #P < 0.01 versus gp120 treatment alone). Interestingly, Z-DEVD-FMK exposure appeared to enhance Tat toxicity at 24 h (bP < 0.05 versus Tat-treated or vehicle-treated cultures). About 50–75 neurons were arbitrarily sampled per culture. At least 4–6 separate cultures, each consisting of cells isolated and maintained from separate mice were assessed per experimental group. Rates of neuronal death in DEVD-FMK treated cultures did not differ significantly from vehicle-treated controls; DEVD = Z-DEVD-FMK.

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