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

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 Ca²⁺ 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.