Cycloheximide and actinomycin D block the toxic effect of glutamic acid on PC12 cells

Neuroreport. 1994 Dec 30;6(1):29-32. doi: 10.1097/00001756-199412300-00009.

Abstract

Programmed cell death is considered to play a key role during development and also during physiopathological events such as neurodegenerative diseases and ischaemia. We have recently shown in PC12 cells that glutamate induces a progressive cytotoxicity which is only visible 8-10 h after incubation with glutamate for at least 4-6 h. We now present evidence that the toxic action of glutamate may correspond to programmed cell death because it is blocked by either actinomycin D or cycloheximide. This effect, however, may not be due to apoptosis since it is not blocked by aurintricarboxylic acid, a non-specific inhibitor of endonucleases, and neither chromatin condensation nor DNA fragmentation or liberation is seen after glutamate treatment.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Aurintricarboxylic Acid / pharmacology
  • Cycloheximide / pharmacology*
  • DNA Damage
  • Dactinomycin / pharmacology*
  • Glutamic Acid / toxicity*
  • PC12 Cells
  • Rats

Substances

  • Dactinomycin
  • Glutamic Acid
  • Aurintricarboxylic Acid
  • Cycloheximide