Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Chronic Histological Outcomes of Indirect Traumatic Optic NEU-Ropathy in Adolescent Mice: Persistent Degeneration and Tem-Porally Regulated Glial Responses

Version 1 : Received: 28 October 2021 / Approved: 4 November 2021 / Online: 4 November 2021 (09:26:51 CET)

A peer-reviewed article of this Preprint also exists.

Hetzer, S.M.; Shalosky, E.M.; Torrens, J.N.; Evanson, N.K. Chronic Histological Outcomes of Indirect Traumatic Optic Neuropathy in Adolescent Mice: Persistent Degeneration and Temporally Regulated Glial Responses. Cells 2021, 10, 3343. Hetzer, S.M.; Shalosky, E.M.; Torrens, J.N.; Evanson, N.K. Chronic Histological Outcomes of Indirect Traumatic Optic Neuropathy in Adolescent Mice: Persistent Degeneration and Temporally Regulated Glial Responses. Cells 2021, 10, 3343.

Journal reference: Cells 2021, 10, 3343
DOI: 10.3390/cells10123343

Abstract

Injury to the optic nerve, termed, traumatic optic neuropathy (TON) is a known comorbidity of traumatic brain injury (TBI) and is now known to cause chronic and progressive retinal thinning up to 35 years after injury. Although animal models of TBI have described the presence of optic nerve degeneration and research exploring acute mechanisms is underway, few studies in humans or animals have examined chronic TON pathophysiology outside the retina. We used a closed-head weight-drop model of TBI/TON in 6-week-old male C57BL/6 mice. Mice were euthanized 7-, 14-, 30-, 90-, and 150-days post injury (DPI) to assess histological changes in the visual system of the brain spanning a total of 12 regions. We show chronic elevation of FluoroJade-C, indicative of neurodegeneration, throughout the time course. Intriguingly, FJ-C staining revealed a bimodal distribution of mice indicating the possibility of subpopulations that may be more or less sus-ceptible to injury outcomes. Additionally, we show that microglia and astrocytes react to optic nerve damage in both temporally and regionally different ways. Despite these differences, as-trogliosis and microglial changes were alleviated between 14-30 DPI in all regions examined, perhaps indicating a potential critical period for intervention/recovery that may determine chronic outcomes.

Keywords

traumatic optic neuropathy; mice; axon injury; TBI; neurodegeneration

Subject

MEDICINE & PHARMACOLOGY, Pathology & Pathobiology

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