6533b85efe1ef96bd12c054f

RESEARCH PRODUCT

Neurotoxicity in Rat Cortical Cells Caused by N-Methyl-D-Aspartate (NMDA) and gp120 of HIV-1: Induction and Pharmacological Intervention

Claudia SchlegerG. PergandeSanja PerovicW. E. G. MüllerH. UshijimaM. Kelve

subject

NeurotoxicityBiologyPharmacologymedicine.diseasechemistry.chemical_compoundmedicine.anatomical_structurePhospholipase A2nervous systemchemistryCerebral cortexApoptosismedicinebiology.proteinNMDA receptorArachidonic acidFragmentation (cell biology)Receptor

description

Incubation of highly enriched neurons from rat cerebral cortex with the human immunodeficiency virus type 1 (HIV-1) coat protein gpl20 for 18 h results in fragmentation of DNA at internucleosomal linkers, a feature of apoptosis. We report that neurons respond to exposure to gp120 with an increased release of arachidonic acid via activation of phospholipase A2. This process is not inhibited by antagonists of the N-methyl-D-aspartate (NMDA) receptor channels. To investigate the influence of arachidonic acid on the sensitivity of NMDA receptor towards its aganist, low concentrations of NMDA were coadministered with arachidonic acid. Under these conditions the NMDA-mediated cytotoxicity was enhanced. We conclude that gp120 causes an activation of phospholipase A2, resulting in an increased release of arachidonic acid which in turn sensitizes the NMDA receptor.

yearjournalcountryeditionlanguage
1996-01-01
https://doi.org/10.1007/978-3-642-79850-4_3