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- Document 0872
- DOCN M9620872
- TI Exposure to gp120 of HIV-1 induces an increased release of arachidonic
- acid in rat primary neuronal cell culture followed by NMDA
- receptor-mediated neurotoxicity.
- DT 9602
- AU Ushijima H; Nishio O; Klocking R; Perovic S; Muller WE; Institute of
- Public Health, Tokyo, Japan.
- SO Eur J Neurosci. 1995 Jun 1;7(6):1353-9. Unique Identifier : AIDSLINE
- MED/96073244
- AB After incubation of highly enriched neurons from rat cerebral cortex
- with the HIV-1 coat protein gp120 for 18 h, cells showed fragmentation
- of DNA at internucleosomal linkers followed by NMDA receptor-mediated
- neurotoxicity. We report that in response to exposure to gp120 cells
- react with an increased release of arachidonic acid (AA) via activation
- of phospholipase A2. This process was not inhibited by NMDA receptor
- antagonists. To investigate the role of AA on the sensitivity of the
- NMDA receptor towards its agonist, low concentrations of NMDA were
- co-administered with AA. This condition enhanced the NMDA-mediated
- cytotoxicity. Administration of mepacrine reduced cytotoxicity caused by
- gp120. We conclude that gp120 causes an activation of phospholipase A2,
- resulting in the increased release of AA, which may in turn sensitize
- the NMDA receptor.
- DE Animal Arachidonic Acid/ANTAGONISTS & INHIB/*METABOLISM Cell Death
- Cells, Cultured DNA Damage/DRUG EFFECTS HIV Envelope Protein
- gp120/*PHARMACOLOGY *HIV-1 Neurons/*DRUG
- EFFECTS/*METABOLISM/PHYSIOLOGY Neurotoxins/*PHARMACOLOGY
- Quinacrine/PHARMACOLOGY Rats Rats, Wistar Receptors,
- N-Methyl-D-Aspartate/ANTAGONISTS & INHIB/*PHYSIOLOGY Support, Non-U.S.
- Gov't JOURNAL ARTICLE
-
- SOURCE: National Library of Medicine. NOTICE: This material may be
- protected by Copyright Law (Title 17, U.S.Code).
-
-