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 language | English |
|---|---|
| Pages (from-to) | 599-609 |
| Number of pages | 11 |
| Journal | Journal of Ocular Pharmacology and Therapeutics |
| Volume | 19 |
| Issue number | 6 |
| State | Published - Dec 2003 |
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All Science Journal Classification (ASJC) codes
- Pharmacology (medical)
- Ophthalmology
- Pharmacology, Toxicology and Pharmaceutics(all)
Cite this
Glucose-Deprivation-Induced [3H]D-Aspartate Release from Isolated Bovine and Human Retinae. / Ohia, Sunny E.; Awe, S. Olubusayo; Opere, Catherine A.; LeDay, Angela M.; Harris, Lydia C.; Kulkarni, Kaustubh; Sharif, Najam A.
In: Journal of Ocular Pharmacology and Therapeutics, Vol. 19, No. 6, 12.2003, p. 599-609.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Glucose-Deprivation-Induced [3H]D-Aspartate Release from Isolated Bovine and Human Retinae
AU - Ohia, Sunny E.
AU - Awe, S. Olubusayo
AU - Opere, Catherine A.
AU - LeDay, Angela M.
AU - Harris, Lydia C.
AU - Kulkarni, Kaustubh
AU - Sharif, Najam A.
PY - 2003/12
Y1 - 2003/12
N2 - 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.
AB - 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.
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M3 - Article
VL - 19
SP - 599
EP - 609
JO - Journal of Ocular Pharmacology and Therapeutics
JF - Journal of Ocular Pharmacology and Therapeutics
SN - 1080-7683
IS - 6
ER -