Abstract
Abstract: :
Purpose: To investigate the orthograde and retrograde axonal transport in retinal ganglion cells (RGCs) after transient ligature of the ophthalmic vessels (LOV). Methods: In adult Sprague-Dawley rats, the left ophthalmic vessels were ligated for 90 minutes. Retrograde axonal transport was investigated by applying the retrogradely transported neuronal tracer Fluorogold (FG) to both superior colliculi 7 days before LOV or 1 hour or 7 days after LOV, and estimating the densities of FG-labelled RGCs in both retinas 7 or 14 days after LOV. Orthograde axonal transport was investigated 30 or 60 days after LOV by injecting 5 days prior to sacrifice, the orthogradely transported tracer cholera toxin subunit B (CTB), in the vitreous of the left eye. Serial coronal sections (40 µm thick) of the midbrain were immuno-stained for CTB. The visual layers of the contralateral superior colliculus (SC) were examined, with the aid of an image analysis system, to determine the extension of areas densely innervated by CTB-labelled RGC terminals. Results: Retrograde transport; 7 days after LOV the densities of FG-labelled RGCs in the ischemic retinas had diminished to 53% or 39% of their contralateral non-ischemic retinas, in the animals in which FG was applied to the SC 7 days before LOV or 1 hour after LOV, respectively. Fourteen days after LOV, the densities of FG-labelled RGCs in the ischemic retinas had diminished to 48% or 27% of their contralateral non-ischemic retinas, in the animals in which FG was applied to the SC 7 days before LOV or 7 days after LOV, respectively. Anterograde transport; In control rats, typical dense CTB-labelling was found spanning the entire visual layers of the right SC. Thirty days after LOV there were small areas devoid of CTB-labelled terminals in the visual layers of the right SC. These areas were larger and more numerous in the animals processed 60 days after LOV. Conclusions: Transient ligature of the ophthalmic vessels for 90 minutes induces, in addition to RGC death; i) an alteration of the retrograde axonal transport in a proportion of surviving RGCs; and ii) an alteration in the anterograde axonal transport that may also be related to RGC death.
Keywords: 448 ischemia • 499 optic flow • 385 degenerations/dystrophies