Glutamate cytotoxicity in a neuronal cell line is blocked by membrane depolarization

Brain Res. 1988 Sep 13;460(1):155-60. doi: 10.1016/0006-8993(88)91216-4.

Abstract

To understand better the proximate mechanism involved in the excitotoxic response to L-glutamate (Glu), we have exploited the Glu receptor present in the N18-RE-105 neuroblastoma-embryonic retinal hybrid cell line. These cells undergo lysis dependent on extracellular Ca2+ when exposed to Glu. We now report that the depolarizing action of Glu is not responsible for its cytotoxic effects. Furthermore, depolarization of these cells with elevated K+, ouabain or veratridine does not cause cytotoxicity but rather protects against the cytotoxic effects of Glu. Our results may implicate a role for voltage-sensitive Ca2+ channels (VSCCs) in cytotoxicity, and depolarization-induced inactivation of VSCCs (Nature (Lond.), 316 (1985) 440-443) as a protection against Glu receptor agonists. Our findings demonstrate a clear dissociation between depolarization and the neuronal degeneration caused by Glu.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cell Line
  • Glutamates / pharmacology*
  • Glutamic Acid
  • Hybrid Cells / physiology
  • Ibotenic Acid / pharmacology
  • Membrane Potentials / drug effects
  • Neuroblastoma
  • Neurons / drug effects
  • Neurons / physiology*
  • Neurotoxins*
  • Oxadiazoles / pharmacology
  • Quisqualic Acid
  • Retina

Substances

  • Glutamates
  • Neurotoxins
  • Oxadiazoles
  • Ibotenic Acid
  • Glutamic Acid
  • Quisqualic Acid