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Text
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URL Address
<a href="http://doi.org/10.1002/cne.24012" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/cne.24012</a>
Pages
3503–3517
Issue
17
Volume
524
Dublin Core
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Title
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Persistence of intact retinal ganglion cell terminals after axonal transport loss in the DBA/2J mouse model of glaucoma.
Publisher
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The Journal of comparative neurology
Date
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2016
2016-12
Subject
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*Axonal Transport/physiology; *bouton; *mitochondria; *neurodegeneration; *retinal; *RRID:IMSRJAX:000671; *RRID:IMSRJAX:007048; *RRID:SCR002716; *RRID:SCR002865; *superior colliculus; *synapse; Animal; Animals; Disease Models; Electron; Glaucoma/metabolism/*pathology; Imaging; Inbred DBA; Mice; Microscopy; Mitochondria/pathology; Neuroanatomical Tract-Tracing Techniques; Regression Analysis; Retinal Ganglion Cells/metabolism/*pathology; Scanning; Superior Colliculi/metabolism/*pathology; Synapses/metabolism/*pathology; Three-Dimensional; Visual Pathways/metabolism/pathology
Creator
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Smith Matthew A; Xia Christina Z; Dengler-Crish Christine M; Fening Kelly M; Inman Denise M; Schofield Brett R; Crish Samuel D
Description
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Axonal transport defects are an early pathology occurring within the retinofugal projection of the DBA/2J mouse model of glaucoma. Retinal ganglion cell (RGC) axons and terminals are detectable after transport is affected, yet little is known about the condition of these structures. We examined the ultrastructure of the glaucomatous superior colliculus (SC) with three-dimensional serial block-face scanning electron microscopy to determine the distribution and morphology of retinal terminals in aged mice exhibiting varying levels of axonal transport integrity. After initial axonal transport failure, retinal terminal densities did not vary compared with either transport-intact or control tissue. Although retinal terminals lacked overt signs of neurodegeneration, transport-intact areas of glaucomatous SC exhibited larger retinal terminals and associated mitochondria. This likely indicates increased oxidative capacity and may be a compensatory response to the stressors that this projection is experiencing. Areas devoid of transported tracer label showed reduced mitochondrial volumes as well as decreased active zone number and surface area, suggesting that oxidative capacity and synapse strength are reduced as disease progresses but before degeneration of the synapse. Mitochondrial volume was a strong predictor of bouton size independent of pathology. These findings indicate that RGC axons retain connectivity after losing function early in the disease process, creating an important therapeutic opportunity for protection or restoration of vision in glaucoma. J. Comp. Neurol. 524:3503-3517, 2016. (c) 2016 Wiley Periodicals, Inc.
Identifier
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<a href="http://doi.org/10.1002/cne.24012" target="_blank" rel="noreferrer noopener">10.1002/cne.24012</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Axonal Transport/physiology
*bouton
*Mitochondria
*neurodegeneration
*retinal
*RRID:IMSRJAX:000671
*RRID:IMSRJAX:007048
*RRID:SCR002716
*RRID:SCR002865
*superior colliculus
*synapse
2016
Animal
Animals
Crish Samuel D
Dengler-Crish Christine M
Department of Anatomy & Neurobiology
Department of Pharmaceutical Sciences
Disease Models
Electron
Fening Kelly M
Glaucoma/metabolism/*pathology
Imaging
Inbred DBA
Inman Denise M
Mice
Microscopy
Mitochondria/pathology
NEOMED College of Medicine
NEOMED College of Pharmacy
Neuroanatomical Tract-Tracing Techniques
Regression Analysis
Retinal Ganglion Cells/metabolism/*pathology
Scanning
Schofield Brett R
Smith Matthew A
Superior Colliculi/metabolism/*pathology
Synapses/metabolism/*pathology
The Journal of comparative neurology
Three-Dimensional
Visual Pathways/metabolism/pathology
Xia Christina Z