Glutamate release in experimental ischaemia of the retina: an approach using microdialysis

J Neurochem. 1992 Jul;59(1):358-63. doi: 10.1111/j.1471-4159.1992.tb08912.x.


A rabbit eye model of neural ischaemia is described that uses an increased pressure in the anterior eye chamber to block the capillary supply to the retina. A microdialysis probe placed very close to the retinal surface was used to monitor release of amino acids during ischaemia. A large (two- to threefold) increase in the release of glutamate and O-phosphoserine (twofold), but not of six other amino acids monitored, occurred during initial ischaemia. During reperfusion after release of intraocular pressure, much larger (five- to 10-fold) increases in the release of these amino acids were observed. Parallel ischaemic retinal tissue damage was observed. This damage was prevented by ketamine applied locally via a superfusion needle, suggesting that glutamate released during ischaemia, and particularly during reperfusion, was responsible for cell death.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acids / metabolism
  • Animals
  • Dialysis / methods
  • Glutamates / metabolism*
  • Glutamic Acid
  • Ischemia / metabolism*
  • Ischemia / pathology
  • Ketamine / pharmacology
  • Male
  • Rabbits
  • Reperfusion
  • Retina / drug effects
  • Retina / metabolism
  • Retina / pathology
  • Retinal Diseases / metabolism
  • Retinal Diseases / pathology
  • Retinal Vessels*


  • Amino Acids
  • Glutamates
  • Glutamic Acid
  • Ketamine