• Retina · Jul 2011

    Phoneutria spider toxins block ischemia-induced glutamate release and neuronal death of cell layers of the retina.

    • 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, and Marcus Vinicius Gomez.
    • Graduation Course in Biomedicine, Santa Casa Hospital, Belo Horizonte, Minas Gerais, Brazil.
    • Retina (Philadelphia, Pa.). 2011 Jul 1;31(7):1392-9.

    PurposeTo investigate the effect of calcium channel blockers, spider toxins, on cell viability and the glutamate content of ischemic retinal slices.MethodsRat 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.ResultsIn 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.ConclusionSpider toxins reduced glutamate content and cell death of retinal ischemic slices.

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