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<a href="http://doi.org/10.1016/j.exer.2015.11.016" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.exer.2015.11.016</a>
Pages
22–33
Volume
150
Dublin Core
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Title
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Early astrocyte redistribution in the optic nerve precedes axonopathy in the DBA/2J mouse model of glaucoma.
Publisher
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Experimental eye research
Date
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2016
2016-09
Subject
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*Astrocyte; *Axonopathy; *Glaucoma; *Gliosis; *Neurodegeneration; *Retinal ganglion cell; Animal; Animals; Astrocytes/*pathology; Axons/pathology; Disease Models; Glaucoma; Imaging; Inbred DBA; Mice; Nerve Degeneration/etiology/*pathology; Open-Angle/*pathology; Optic Nerve Diseases/etiology/*pathology; Optic Nerve/*pathology; Photomicrography; Retinal Ganglion Cells/*pathology; Three-Dimensional; Time Factors
Creator
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Cooper Melissa L; Crish Samuel D; Inman Denise M; Horner Philip J; Calkins David J
Description
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Glaucoma challenges the survival of retinal ganglion cell axons in the optic nerve through processes dependent on both aging and ocular pressure. Relevant stressors likely include complex interplay between axons and astrocytes, both in the retina and optic nerve. In the DBA/2J mouse model of pigmentary glaucoma, early progression involves axonopathy characterized by loss of functional transport prior to outright degeneration. Here we describe novel features of early pathogenesis in the DBA/2J nerve. With age the cross-sectional area of the nerve increases; this is associated generally with diminished axon packing density and survival and increased glial coverage of the nerve. However, for nerves with the highest axon density, as the nerve expands mean cross-sectional axon area enlarges as well. This early expansion was marked by disorganized axoplasm and accumulation of hyperphosphorylated neurofilamants indicative of axonopathy. Axon expansion occurs without loss up to a critical threshold for size (about 0.45-0.50 mum(2)), above which additional expansion tightly correlates with frank loss of axons. As well, early axon expansion prior to degeneration is concurrent with decreased astrocyte ramification with redistribution of processes towards the nerve edge. As axons expand beyond the critical threshold for loss, glial area resumes an even distribution from the center to edge of the nerve. We also found that early axon expansion is accompanied by reduced numbers of mitochondria per unit area in the nerve. Finally, our data indicate that both IOP and nerve expansion are associated with axon enlargement and reduced axon density for aged nerves. Collectively, our data support the hypothesis that diminished bioenergetic resources in conjunction with early nerve and glial remodeling could be a primary inducer of progression of axon pathology in glaucoma.
Identifier
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<a href="http://doi.org/10.1016/j.exer.2015.11.016" target="_blank" rel="noreferrer noopener">10.1016/j.exer.2015.11.016</a>
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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).
*Astrocyte
*Axonopathy
*Glaucoma
*Gliosis
*neurodegeneration
*Retinal ganglion cell
2016
Animal
Animals
Astrocytes/*pathology
Axons/pathology
Calkins David J
Cooper Melissa L
Crish Samuel D
Department of Pharmaceutical Sciences
Disease Models
Experimental eye research
Glaucoma
Horner Philip J
Imaging
Inbred DBA
Inman Denise M
Mice
NEOMED College of Pharmacy
Nerve Degeneration/etiology/*pathology
Open-Angle/*pathology
Optic Nerve Diseases/etiology/*pathology
Optic Nerve/*pathology
Photomicrography
Retinal Ganglion Cells/*pathology
Three-Dimensional
Time Factors