Anatomical and Molecular Responses Triggered in the Retina by Axonal Injury

Agudo‐Barriuso, Marta; Nadal-Nicolás, Francisco M.; Parrilla–Reverter, G.; Villegas‐Pérez, María Paz; Vidal‐Sanz, Manuel

doi:10.5772/19066

Cited by 1 publication

(1 citation statement)

References 92 publications

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“…Similarly, optic nerve levels of both NEFL and NEFH are decreased 0.5 hours to 3 days after optic nerve stretch in mice [ 30 ]. Thus, our finding of decreased levels of NEFL, NEFM, NEHP and also PRPH and INA proteins is in line with several works showing changes in neurofilaments in optic nerve and retina after optic nerve injury; for a detailed review see Agudo-Barrioso et al 2011 [ 31 ].…”

Section: Discussionsupporting

confidence: 91%

Sub-Chronic Neuropathological and Biochemical Changes in Mouse Visual System after Repetitive Mild Traumatic Brain Injury

et al. 2016

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Repetitive mild traumatic brain injury (r-mTBI) results in neuropathological and biochemical consequences in the human visual system. Using a recently developed mouse model of r-mTBI, with control mice receiving repetitive anesthesia alone (r-sham) we assessed the effects on the retina and optic nerve using histology, immunohistochemistry, proteomic and lipidomic analyses at 3 weeks post injury. Retina tissue was used to determine retinal ganglion cell (RGC) number, while optic nerve tissue was examined for cellularity, myelin content, protein and lipid changes. Increased cellularity and areas of demyelination were clearly detectable in optic nerves in r-mTBI, but not in r-sham. These changes were accompanied by a ~25% decrease in the total number of Brn3a-positive RGCs. Proteomic analysis of the optic nerves demonstrated various changes consistent with a negative effect of r-mTBI on major cellular processes like depolymerization of microtubules, disassembly of filaments and loss of neurons, manifested by decrease of several proteins, including neurofilaments (NEFH, NEFM, NEFL), tubulin (TUBB2A, TUBA4A), microtubule-associated proteins (MAP1A, MAP1B), collagen (COL6A1, COL6A3) and increased expression of other proteins, including heat shock proteins (HSP90B1, HSPB1), APOE and cathepsin D. Lipidomic analysis showed quantitative changes in a number of phospholipid species, including a significant increase in the total amount of lysophosphatidylcholine (LPC), including the molecular species 16:0, a known demyelinating agent. The overall amount of some ether phospholipids, like ether LPC, ether phosphatidylcholine and ether lysophosphatidylethanolamine were also increased, while the majority of individual molecular species of ester phospholipids, like phosphatidylcholine and phosphatidylethanolamine, were decreased. Results from the biochemical analysis correlate well with changes detected by histological and immunohistochemical methods and indicate the involvement of several important molecular pathways. This will allow future identification of therapeutic targets for improving the visual consequences of r-mTBI.

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Section: Discussionsupporting

confidence: 91%