Calbindin D28K-containing neurons, and not HSP70-expressing neurons, are more resistant to HIV-1 envelope (gp120) toxicity in cortical cell cultures.

HIV-1-associated cognitive/motor complex is one of the major neurological complications of AIDS and is associated with neuronal loss. Gp120, the HIV envelope protein, is toxic for neurons in cultures and produces a rise in intracytosolic calcium. This neurotoxicity is dose-dependent and time-dependent. We evaluated the selective gp120 toxicity in primary neuronal cultures for calbindin-free and calbindin-containing neurons with semi-quantitative immunocytochemistry using an anti-calbindin D28K monoclonal antibody. The number of immunolabelled neurons was inversely correlated to neuronal survival. In cultures exposed to gp120 (100 pM) for 24 hr the neuronal survival of initial platings was 19.7 +/- 2.1% and the percentage of neuronal survival was 84.6 +/- 4.9% in control cultures exposed to the vehicle. The corresponding percentages of immunolabelled neurons were 85.0 +/- 2.1% in treated cultures and 23.6 +/- 3.1% in control cultures (P < 0.001). The expression of heat shock proteins by heating cell cultures did not protect neurons from gp120 toxicity. These results suggest that calbindin D2K28-containing neurons are more resistant to gp120-toxicity in this cell culture system.