Human, bovine, and rabbit retinal glutamate-induced [3H]D-aspartate release: role in excitotoxicity

Neurochem Res. 2000 Jun;25(6):853-60. doi: 10.1023/a:1007525725996.


The pharmacological basis of glutamate-induced [3H]D-aspartate release was investigated in isolated human, bovine and rabbit retinas. Isolated mammalian retinas were preloaded with [3H]D-aspartate and then prepared for studies of neurotransmitter release using the superfusion method. Release of [3H]D-aspartate was elicited by K+ (50 mM) or by L-glutamate. In bovine retinas, L-glutamate, but not D-glutamate induced an overflow of [3H]D-aspartate that was partially inhibited by low external calcium, omega-conotoxin (10 nM) or nitrendipine (1 microM). Metabotropic glutamate receptor (GLUR) agonists also evoked [3H]D-aspartate release in both bovine and human retinas whereas polyamines only enhanced the excitatory effects of L-glutamate on [3H]D-aspartate release. Antagonists of GLURs and the polyamine site inhibited L-glutamate evoked [3H]D-aspartate overflow with the following rank order of potency: MCPG >ifenprodil > AP-5 > arcaine> MK-801. In conclusion, L-glutamate-induces a stereoselective, calcium-dependent release of [3H]D-aspartate from isolated mammalian retinas that can be mimicked by GLUR agonists (and blocked by both receptor and polyamine site antagonists).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Animals
  • Aspartic Acid / metabolism*
  • Cattle
  • Excitatory Amino Acid Agonists / pharmacology
  • Glutamic Acid / pharmacology*
  • Humans
  • Middle Aged
  • Rabbits
  • Receptors, Metabotropic Glutamate / agonists
  • Retina / drug effects*
  • Retina / metabolism
  • Tritium


  • Excitatory Amino Acid Agonists
  • Receptors, Metabotropic Glutamate
  • Tritium
  • Aspartic Acid
  • Glutamic Acid