Glucose-Deprivation-Induced [3H]D-Aspartate Release from Isolated Bovine and Human Retinae

Sunny E. Ohia, S. Olubusayo Awe, Catherine A. Opere, Angela M. LeDay, Lydia C. Harris, Kaustubh Kulkarni, Najam A. Sharif

Research output: Contribution to journalArticle

3 Scopus citations

Abstract

The glucose deprivation-induced release of [3H]D-aspartate was studied in bovine and human retinas in a superfusion apparatus. [ 3H]D-aspartate release was significantly increased upon omitting glucose in the superfusion buffer. This effect was dependent on external Ca 2+ because L- and N-type Ca2+-channel blockers, such as diltiazem (1 μM), nitrendipine (1 μM), and ω-conotoxin (100 nM), significantly reduced the effect of glucose-deprivation induced release of [3H]D-aspartate. Furthermore, while glutamate receptor agonists (L-glutamate, N-methyl-D-aspartate, but not kainate) potentiated the effects of glucose deprivation, antagonists (MK-801, MCPG, ifenprodil, and L-AP3) at these receptors blocked the glucose deprivation-induced release process. Taken together, these studies have demonstrated that under conditions of glucose deprivation, as may happen during ischemic events in vivo, the retinal glutamatergic nerve endings and/or glial cells promote the efflux of [ 3H]D-aspartate into the extracellular environment. This process appears to be receptor-mediated and dependent on extracellular Ca2+ and is similar to previous reports pertaining to brain tissues.

Original languageEnglish (US)
Pages (from-to)599-609
Number of pages11
JournalJournal of Ocular Pharmacology and Therapeutics
Volume19
Issue number6
DOIs
StatePublished - Dec 2003

All Science Journal Classification (ASJC) codes

  • Ophthalmology
  • Pharmacology
  • Pharmacology (medical)

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