Tissue-type plasminogen activator is not required for kainate-induced motoneuron death in vitro

Neuroreport. 1998 Aug 24;9(12):2791-6. doi: 10.1097/00001756-199808240-00020.

Abstract

Spinal motoneurons are highly vulnerable to kainate both in vivo and in vitro. Tissue-type plasminogen activator (tPA) and plasmin have recently been shown to mediate kainate-induced neuronal death in the mouse hippocampus in vivo. The aim of the present study was to determine whether tPA also mediates the kainate-induced death of motoneurons in vitro. A motoneuron-enriched neuronal population was isolated from the ventral spinal cord of wild-type (WT) and tPA-deficient (tPA-/-) mouse embryos. WT and tPA-/- neurons were cultured on WT and tPA-/- spinal glial feeder layers, respectively. WT and tPA-/- co-cultures were morphologically indistinguishable. Expression of tPA in WT co-cultures was demonstrated using RT-PCR. WT and tPA-/- co-cultures were exposed to kainate for 24 h. The neurotoxic effect of kainate did not differ significantly between WT and tPA-/- cultures. The plasmin inhibitor alpha2-antiplasmin did not protect WT neurons against kainate-induced injury. These results indicate that the plasmin system is not a universal mediator of kainate-induced excitotoxicity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Death / drug effects
  • Cells, Cultured
  • Coculture Techniques
  • Excitatory Amino Acid Agonists / toxicity*
  • Fibrinolysin / physiology
  • Immunohistochemistry
  • Kainic Acid / toxicity*
  • Mice
  • Motor Neurons / drug effects*
  • Neuroglia / physiology
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • Receptors, AMPA / drug effects
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tissue Plasminogen Activator / deficiency
  • Tissue Plasminogen Activator / physiology*

Substances

  • Excitatory Amino Acid Agonists
  • RNA, Messenger
  • Receptors, AMPA
  • Tissue Plasminogen Activator
  • Fibrinolysin
  • Kainic Acid