Autor: |
Mitton, K.P., Deshpande, M., Wong, S.C., Guzman, E., Cheng, M., Dailey, W., Schunemann, R., Trese, M., Drenser, K. |
Jazyk: |
angličtina |
Rok vydání: |
2019 |
Předmět: |
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DOI: |
10.1101/2019.12.12.874271 |
Popis: |
Purpose Bipolar cells can perish during inner retinal ischemia resulting from disruption of the inner retinal microvasculature. Can surviving inner retinal neurons recover and integrate into the functional network after ischemic damage? Using the mouse oxygen induced retinopathy (OIR) model, we applied focal-ERG to determine if B-wave recovery occurs after ischemic bipolar cell death after revascularization. Methods The OIR model was used to generate regions of inner retinal neuron loss in B6.Cg-Tg Thy1-YFP mice. Using image-guided focal-ERG, the dark-adapted mixed rod-cone light response was compared using stimulation of small circular (0.27 mm diameter) target areas located in the central retinas of the same eyes (OIR and control). The same areas of the same retinas were followed over three ages after revascularization (P21, P28 and P42). Results There was a minimal effect on the photoreceptor-derived A-wave amplitude in the central damaged regions. B-wave amplitudes were almost absent in these damaged central regions at age P21, and progressively recovered through ages P28 to P42. The magnitude of the recovered B-wave amplitude by P42 remained less than the normal control retina (room air), but did show oscillatory potentials. Conclusions Recovery of retinal functionality, a neural plasticity, was detected in the central damaged regions of the mouse OIR model after the initial loss of bipolar cells and revascularization of these zones. These results suggest that any treatments that would enhance the overall survival of inner retinal neurons result in a significant improvement in neural function after any surviving neurons establish connectivity. |
Databáze: |
OpenAIRE |
Externí odkaz: |
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