Journal
EXPERIMENTAL NEUROLOGY
Volume 215, Issue 2, Pages 253-263Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.expneurol.2008.10.006
Keywords
HIV-1 Tat; Neuronal cell culture; Toxicity; Caspases; MCP-1; NMDAR
Categories
Funding
- NICHD NIH HHS [HD 43680, R01 HD043680, R01 HD043680-04] Funding Source: Medline
- NIDA NIH HHS [DA 09160, R03 DA031604, R01 DA009160-07, DA 11337, R01 DA011337-03, DA 13137, R01 DA013137-09, R01 DA013137] Funding Source: Medline
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In this study we report that primary cultures of rat fetal neurons contain subpopulations of cells that may be sensitive or resistant to HIV-1 Tat neurotoxicity. We demonstrate that rapid binding/uptake of Tat 1-86 for 2 h was sufficient to trigger caspase activation and neurodegeneration in rat fetal midbrain cell cultures. The uptake of Tat was followed by an increase in MCPI (CCL2) immunoreactivity. Approximately 70% of neurons were able to survive transient or Continuous (7 days) Tat exposure. The surviving neurons did not contain bound/internalized Tat, but were able to interact with Tat after medium replacement. These neurons were resistant to Tat toxicity. In neurons that resisted the toxic effects of continuous and repeated Tat treatment, levels of NR2A subunit of the NMDA receptor complex were significantly lower than in controls. We suggest that the subunit composition of NMDAR complexes may be important for the sensitivity of neurons to Tat toxicity. (c) 2008 Elsevier Inc. All rights reserved.
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