Journal of NeuroVirology

, Volume 15, Issue 5, pp 401–410

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
Article

DOI: 10.3109/13550280903296346

Cite this article as:
Hu, S., Sheng, W.S., Lokensgard, J.R. et al. Journal of NeuroVirology (2009) 15: 401. doi:10.3109/13550280903296346

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.

Keywords

dopaminegp120neuronsoxidative stress

Copyright information

© Journal of NeuroVirology, Inc. 2009

Authors and Affiliations

  • Shuxian Hu
    • 1
  • Wen S. Sheng
    • 1
  • James R. Lokensgard
    • 1
  • Phillip K. Peterson
    • 1
  • R. Bryan Rock
    • 1
  1. 1.Center for Infectious Diseases and Microbiology Translational Research, Division of Infectious Diseases and International Medicine, Department of MedicineUniversity of Minnesota Medical SchoolMinneapolisUSA