HIV-1-associated cognitive/motor dysfunction is a frequent neurologica
l complication of acquired immunodeficiency syndrome (AIDS) and has be
en termed AIDS dementia complex (ADC). The HIV-1 envelope glycoprotein
gp120 has been implicated in producing brain injury associated with A
DC. The purpose of the present study was to determine if gp120-induced
neurotoxicity is associated with damage to dopaminergic systems. Expo
sure of rat midbrain dopamine cultures to gp120 for 3 days reduced the
ability of dopaminergic cells to transport this amine and also result
ed in a reduction in dopamine neuron process length while it did not a
lter either dopamine cell number or the total number of neuronal cells
. These detrimental effects of gp120 were prevented by an NMDA recepto
r antagonist (MK-801) or by preincubation with anti-gp120 antibody. Th
ese results suggest that dopaminergic neuronal damage may contribute t
o the manifestations of AIDS dementia complex.