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

S. E. Ohia, C. A. Opere, S. Olubusayo Awe, L. Adams, N. A. Sharif

Research output: Contribution to journalArticlepeer-review

16 Scopus citations

Abstract

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, ω-conotoxin (10 nM) or nitrendipine (1 μM). 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).

Original languageEnglish (US)
Pages (from-to)853-860
Number of pages8
JournalNeurochemical Research
Volume25
Issue number6
DOIs
StatePublished - Jan 1 2000

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Cellular and Molecular Neuroscience

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