HIV-1 gp120-induced neurotoxicity to midbrain dopamine cultures

Barbara A. Bennett, Daniel E. Rusyniak, Charlotte K. Hollingsworth

Research output: Contribution to journalArticle

77 Scopus citations


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

Original languageEnglish (US)
Pages (from-to)168-176
Number of pages9
JournalBrain research
Issue number1-2
StatePublished - Dec 24 1995
Externally publishedYes


  • Dopamine uptake
  • HIV-1
  • Midbrain culture
  • NMDA
  • Neurotoxicity
  • gp120

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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