Abstract | PURPOSE: METHODS: Rat retinal slices were subjected to ischemia via exposure to oxygen-deprived low- glucose medium for 45 minutes. Slices were either treated or not treated with the toxins PhTx3, Tx3-3, and Tx3-4. After oxygen-deprived low- glucose insult, glutamate content and cell viability were assessed in the slices by confocal and optical microscopy. RESULTS: In the retinal ischemic slices that were treated with PhTx3, Tx3-3, and Tx3-4, confocal imaging showed a decrease in cell death of 79.5 ± 3.1%, 75.5 ± 5.8%, and 61 ± 3.8%, respectively. Neuroprotective effects were also observed 15, 30, 60, and 90 minutes after the onset of the retinal ischemic injury. As a result of the ischemia, glutamate increased from 6.2 ± 1.0 nMol/mg protein to 13.2 ± 1.0 nMol/mg protein and was inhibited by PhTx3, Tx3-3, and Tx3-4 to 8.6 ± 0.7, 8.8 ± 0.9, and 7.4 ± 0.8 nMol/mg protein, respectively. Histologic analysis of the live cells in the outer, inner, and ganglion cell layers of the ischemic slices showed a considerable reduction in cell death by the toxin treatment. CONCLUSION:
|
Authors | Rafael Mourão Agostini, Ana Cristina do Nascimento Pinheiro, Nancy Scardua Binda, Marco Aurélio Romano Silva, Marta do Nascimento Cordeiro, Michael Richardson, André Luiz Sena Guimarães, Marcus Vinicius Gomez |
Journal | Retina (Philadelphia, Pa.)
(Retina)
2011 Jul-Aug
Vol. 31
Issue 7
Pg. 1392-9
ISSN: 1539-2864 [Electronic] United States |
PMID | 21394062
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
|
Chemical References |
- Calcium Channel Blockers
- Neuropeptides
- Neuroprotective Agents
- Neurotoxins
- Spider Venoms
- Tx3 neurotoxin
- Glutamic Acid
|
Topics |
- Animals
- Calcium Channel Blockers
(pharmacology)
- Cell Death
(drug effects)
- Cell Survival
(drug effects)
- Glutamic Acid
(metabolism)
- Microscopy, Confocal
- Neuropeptides
(pharmacology)
- Neuroprotective Agents
(pharmacology)
- Neurotoxins
(pharmacology)
- Rats
- Rats, Wistar
- Reperfusion Injury
(metabolism, prevention & control)
- Retinal Diseases
(metabolism, prevention & control)
- Retinal Neurons
(drug effects)
- Spider Venoms
(pharmacology)
|