Time-Dependent Effects of Focal Retinal Ischemia on Axonal Cytoskeleton Proteins

Abstract

An ischemic insult induces RGC cytoskeleton protein change, implying that the local environment plays an important role in modulating axonal structure and function. Cytoskeleton proteins are likely to be important pathogenic mediators of neuronal dysfunction in diseases such as glaucoma and retinal vascular disease.

Vitreal IgM Autoantibodies Target Neurofilament Medium in a Spontaneous Model of Autoimmune Uveitis

“…Our findings in equine retina place NF-M distribution in the horse very close to that in the pig, which is an established model organism in human glaucoma research. 20,[33][34][35] In the porcine retina, NF-M is also predominantly expressed in RGC axons, dendrites, and cell bodies, with smaller RGC somata staining less frequently. The NF-M signal in the OPL that was also detected in the pig has been attributed to horizontal cells.…”

Evidence for an enduring ischaemic penumbra following central retinal artery occlusion, with implications for fibrinolytic therapy

“…These volumes might be anticipated to be similar in each instance as the effects of orthograde and retrograde transport obstruction are much the same on each side of axonal injury sites generally (Banks et al, 1969;Griffin et al, 1977;Kanamori et al, 2012). The disparity at the optic disc suggests that mitochondrial transportation is very limited within the myelinated portion of an RGC axon, consistent with the much reduced concentration of cytoskeletal components within the retrolaminar optic nerve (Barron et al, 2004;Balaratnasingam et al, 2009Balaratnasingam et al, , 2010; Yu-Wai-Man et al, 2011). The disparity may also Fig.…”

Glaucoma and ocular blood flow: an anatomical perspective

“…In vitro models have shown that neuroprotection of the ischemic RGCs can be obtained through blockage of both of the N-methyl-d-aspartate and non-N-methyl-d-aspartate glutamate receptors, or by the delivery of a minimal amount of glucose [46]. During ischemia, RGC cytoskeleton components have been shown to suffer derangements and could be an important cause of neuronal dysfunction [47]. In addition, these changes are observed before the signs of apoptosis within the RGCs.…”