Wallerian Degeneration of the Optic Nerve in Light of Histological and Biochemical Studies1

Wender, M; Kozik, M; Adamczewska-Goncerzewicz, Z; Goncerzewicz, A

doi:10.1007/978-3-642-81553-9_11

Cited by 5 publications

(1 citation statement)

References 2 publications

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“…Although PC, PE, and PI had different abundance in our samples (56.6%, 27.6% and 3.6%, of the total amount of ester lipids respectively), they appeared to demonstrate the same tendency for a decrease to a similar extent after injury (-22.0%, -21.5% and -23%, respectively). This tendency for a decrease in these phospholipid classes differs from the changes observed after rabbit optic nerve transection, where PC and PE were significantly increased at a similar time point [ 82 ]. As all of these three ester lipid classes are major structural components of myelin, and given the localized nature of the lesion, it is not surprising that they show a tendency to be reduced to a similar extent, however, this change did not show statistical significance.…”

Section: Discussionmentioning

confidence: 76%

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: Discussionmentioning

confidence: 76%