Preferential sensitivity of human dopaminergic neurons to gp120-induced oxidative damage

Shuxian Hu, Wen S. Sheng, James R. Lokensgard, Phillip K. Peterson, R. Bryan Rock

Research output: Contribution to journalArticlepeer-review

29 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)401-410
Number of pages10
JournalJournal of neurovirology
Volume15
Issue number5-6
DOIs
StatePublished - Dec 12 2009

Bibliographical note

Funding Information:
This work has been presented in part at the 14th Annual Conference of the Society on NeuroImmune Pharmacology, Charleston, South Carolina; March 12–16, 2008; no. T-33. This work was supported in part by U.S. Public Health Service grant DA025525.

Keywords

  • Dopamine
  • Gp120
  • Neurons
  • Oxidative stress

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