dc.contributor.author | Bernardo-Colon, Alexandra | |
dc.contributor.author | Vest, Victoria | |
dc.contributor.author | Cooper, Melissa L. | |
dc.contributor.author | Naguib, Sarah A. | |
dc.contributor.author | Calkiins, David J. | |
dc.contributor.author | Rex, Tonia S. | |
dc.date.accessioned | 2019-09-25T15:39:19Z | |
dc.date.available | 2019-09-25T15:39:19Z | |
dc.date.issued | 2019-07-11 | |
dc.identifier.citation | Bernardo-Colón Alexandra, Vest Victoria, Cooper Melissa L., Naguib Sarah A., Calkins David J., Rex Tonia S.
Progression and Pathology of Traumatic Optic Neuropathy From Repeated Primary Blast Exposure,
Frontiers in Neuroscience, 13 , 2019, 719 | en_US |
dc.identifier.issn | 1662-453X | |
dc.identifier.uri | http://hdl.handle.net/1803/9536 | |
dc.description.abstract | Indirect traumatic optic neuropathy (ITON) is a condition that is often associated with traumatic brain injury and can result in significant vision loss due to degeneration of retinal ganglion cell (RGC) axons at the time of injury or within the ensuing weeks. We used a mouse model of eye-directed air-blast exposure to characterize the histopathology of blast-induced ITON. This injury caused a transient elevation of intraocular pressure with subsequent RGC death and axon degeneration that was similar throughout the length of the optic nerve (ON). Deficits in active anterograde axon transport to the superior colliculus accompanied axon degeneration and first appeared in peripheral representations of the retina. Glial area in the ON increased early after injury and involved a later period of additional expansion. The increase in area involved a transient change in astrocyte organization independent of axon degeneration. While levels of many cytokines and chemokines did not change, IL-1 alpha and IL-1 beta increased in both the ON and retina. In contrast, glaucoma shows distal to proximal axon degeneration with astrocyte remodeling and increases in many cytokines and chemokines. Further, direct traumatic optic neuropathies have a clear site of injury with rapid, progressive axon degeneration and cell death. These data show that blast-induced ITON is a distinct neuropathology from other optic neuropathies. | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | FRONTIERS IN NEUROSCIENCE | en_US |
dc.rights | open-access article distributed under the terms of the Creative Commons Attribution
License (CC BY). The use, distribution or reproduction in other forums is permitted,
provided the original author(s) and the copyright owner(s) are credited and that the
original publication in this journal is cited, in accordance with accepted academic
practice. No use, distribution or reproduction is permitted which does not comply
with these terms.
Frontiers in | |
dc.source.uri | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6637732/ | |
dc.subject | optic neuropathy | en_US |
dc.subject | axon degeneration | en_US |
dc.subject | axonopathy | en_US |
dc.subject | blast | en_US |
dc.subject | indirect traumatic optic neuropathy | en_US |
dc.subject | repeat neurotrauma | en_US |
dc.subject | intraocular pressure | en_US |
dc.subject | retinal ganglion cells | en_US |
dc.subject | mouse model | en_US |
dc.subject | human eye | en_US |
dc.subject | axonopathy | en_US |
dc.subject | injury | en_US |
dc.subject | neuroinflammation | en_US |
dc.subject | neurodegeneration | en_US |
dc.subject | redistribution | en_US |
dc.subject | vision | en_US |
dc.subject.lcsh | Intraocular pressure. | en_US |
dc.title | Progression and Pathology of Traumatic Optic Neuropathy From Repeated Primary Blast Exposure | en_US |
dc.type | Article | en_US |
dc.identifier.doi | 10.3389/fnins.2019.00719 | |