Abstract
In this study, we report that partial unilateral optic nerve crush in the rat affects the number of retinal ganglion cells of the contralateral eye still in continuity with the ipsilateral superior colliculus. The reduction in cell number of the uncrossed retinal projection was accompanied by a microglia response and could be prevented by the local intravitreal application of the anti-inflammatory agent dexamethasone. Interestingly, the level of neuronal activity after optic nerve crush as evidenced by thallium autometallography was enhanced in the termination area of the uncrossed projection, the rostro-medial superior colliculus, suggesting that a dying-back mechanism is not involved. We propose that injury signals from the damaged optic nerve and retina are transduced to the unaffected eye.
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