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X. Yang, V. Porciatti; Impairment of Retinal Ganglion Cell Function After Superior Colliculus Ablation in Adult Mice. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5485.
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© ARVO (1962-2015); The Authors (2016-present)
Lesions to the superior colliculus (SC) in neonatal rodents result in rapid death of retinal ganglion cells (RGC). By contrast, SC ablation in adult rodents does not cause obvious anatomical damage even after many months. SC ablation, however, is expected to reduce the amount of retrogradely transported neurotrophic factors that may influence RGC function and survival in disease. We tested the hypothesis that SC ablation in adult mice causes impairment of RGC electrical responsiveness as measured by pattern electroretinogram (PERG).
C57BL/6J mice aged 7-8 months (n=9) were anesthetized with a single I.P. injection of urethane 20% (8 ml/Kg), and the PERG was recorded from either eye. The bone overlying the right SC (0.5 mm lateral to the central suture, 2.9 mm posterior to the bregma) was then drilled to expose the brain and mechanically destroy the SC with a syringe needle. The PERG was sequentially recorded from either eye over the course of 5 hours after SC ablation; mice were then euthanized, and eyes and brain harvested for histological examination.
During the first hour after SC ablation, the PERG amplitude was similar in the two eyes and comparable to pre-surgical baseline values. Between 2 and 3 hours after surgery, the PERG amplitude significantly (P<0.01) decreased by about 50-60% compared to baseline and remained stable at lower levels thereafter. In the eye contralateral to the ablated SC, the PERG amplitude of the ipsilateral eye did not significantly change in the post-surgical period
SC ablation induces rapid decrease of PERG signal in the eye contralateral to the lesion, the temporal dynamics of the effect being consistent with the reported rates of retrograde axonal transport and length of the retino-collicular pathway of mice. Results suggest that continuous support of retrogradely transported factors is necessary for normal RGC responsiveness. Results are relevant for glaucoma, as the exact role of altered axonal transport in glaucomatous optic nerve damage is not known.
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