AURINTRICARBOXYLIC ACID PROTECTS HIPPOCAMPAL-NEURONS FROM GLUTAMATE EXCITOTOXICITY INVITRO

Aurintricarboxylic acid (ATA), an endonuclease inhibitor, has been sho wn to protect several cell types from an apoptotic form of cell death. We tested ATA for protective effects against glutamate excitotoxicity in 2-week-old cultured hippocampal neurons. Cell viability was determ ined 24 h after glutamate exposure either by trypan blue exclusion or by measurement of lactate dehydrogenase release. When ATA was added du ring exposure to glutamate, there was a dramatic increase in the numbe r of viable neurons compared with cultures that did not receive ATA. I f ATA was added after glutamate exposure, the rate of survival approac hed 100%. Several cellular processes may be the targets for ATA action . If the mechanisms of ATA protection are similar for excitotoxicity a nd apoptosis, then these distinct forms of cell death may share a comm on intracellular pathway.