TABLE 1.

Effects of Tat_1-72 or gp120 and caspase inhibition on striatal neuron viability at 24 h following viral protein exposure. gp120 treatment caused significant neuronal losses at 24 h that could be significantly attenuated by pretreating cultures with the caspase inhibitor, Z-DEVD-FMK (DEVD)^a

Treatment	Non-viable neurons (%)b
Vehicle-treated controls	0.84 ± .37
DEVD (50 µM)	0.67 ± .41
HIV-1 Tat1-72 (100nM)	1.00 ± .38
HIV-1 Tat1-72 (100 nM) + DEVD (50 µM)	1.17 ± .24
HIV-1 gp120 (500 pM)	1.71 ±.31*
HIV-1 gp120 (500 pM) + DEVD (50 µM)	0.60 ±.33

^aStriatal neurons were continuously exposed to HIV-1 proteins and/or the soluble caspase inhibitor Z-DEVD-FMK (DEVD) and assayed at 24 h in vitro.

^bNeuronal viability was assessed by determining the proportion of neuronal nuclear (NeuN) immunoreactive neurons that failed to exclude ethidium monoazide (EMA) following 30 min incubation in EMA (see Fig. 3); percentage non-viable neurons = [(EMA and NeuN-positive neurons)/(total NeuN-positive neurons) * 100].

^*P < 0.05 versus vehicle-treated control or gp120-treated cultures.