Open AccessPreferential sensitivity of human dopaminergic neurons to gp120-induced oxidative damage
Author(s) -
Shuxian Hu,
Wen S. Sheng,
James R. Lokensgard,
Phillip K. Peterson,
R. Bryan Rock
Publication year - 2009
Publication title -
journal of neurovirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.868
H-Index - 85
eISSN - 1538-2443
pISSN - 1355-0284
DOI - 10.3109/13550280903296346
Subject(s) - dopaminergic , microglia , dopamine , neurotoxicity , neuroscience , biology , neurodegeneration , midbrain , striatum , microbiology and biotechnology , central nervous system , immunology , medicine , inflammation , toxicity , disease
The dopamine (DA)-rich midbrain is known to be a key target of human immunodeficiency virus (HIV)-1. Studies of simian immunodeficiency virus (SIV)-induced neuropathogenesis recently established that there is a major disruption within the nigrostriatal dopaminergic system characterized by marked depletion of dopaminergic neurons, microglial cell activation, and reactive astrocytes. Using a human mesencephalic neuronal/glial culture model, which contains dopaminergic neurons, microglia, and astrocytes, experiments were performed to characterize the damage to dopaminergic neurons induced by HIV-1 gp120. Functional impairment was assessed by DA uptake, and neurotoxicity was measured by apoptosis and oxidative damage. Through the use of this mesencephalic neuronal/glial culture model, we were able to identify the relative sensitivity of dopaminergic neurons to gp120-induced damage, manifested as reduced function (decreased DA uptake), morphological changes, and reduced viability. We also showed that gp120-induced oxidative damage is involved in this neuropathogenic process.