1
40
2
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Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.neuroscience.2018.08.016" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.neuroscience.2018.08.016</a>
Pages
104–118
Volume
390
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Nodes of Ranvier in Glaucoma.
Publisher
An entity responsible for making the resource available
Neuroscience
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-10
Subject
The topic of the resource
*axonopathy; *axons; *neurodegeneration; *neurofilament; *node of Ranvier; *superior colliculus
Creator
An entity primarily responsible for making the resource
Smith M A; Plyler E S; Dengler-Crish C M; Meier J; Crish S D
Description
An account of the resource
Retinal ganglion cell axons of the DBA/2J mouse model of glaucoma, a model characterized by extensive neuroinflammation, preserve synaptic contacts with their subcortical targets for a time after onset of anterograde axonal transport deficits, axon terminal hypertrophy, and cytoskeletal alterations. Though retrograde axonal transport is still evident in these axons, it is unknown if they retain their ability to transmit visual information to the brain. Using a combination of in vivo multiunit electrophysiology, neuronal tract tracing, multichannel immunofluorescence, and transmission electron microscopy, we report that eye-brain signaling deficits precede transport loss and axonal degeneration in the DBA/2J retinal projection. These deficits are accompanied by node of Ranvier pathology - consisting of increased node length and redistribution of the voltage-gated sodium channel Nav1.6 that parallel changes seen early in multiple sclerosis (MS) axonopathy. Further, with age, axon caliber and neurofilament density increase without corresponding changes in myelin thickness. In contrast to these findings in DBA/2J mice, node pathologies were not observed in the induced microbead occlusion model of glaucoma - a model that lacks pre-existing inflammation. After one week of systemic treatment with fingolimod, an immunosuppressant therapy for relapsing-remitting MS, DBA/2J mice showed a substantial reduction in node pathology and mild effects on axon morphology. These data suggest that neurophysiological deficits in the DBA/2J may be due to defects in intact axons and targeting node pathology may be a promising intervention for some types of glaucoma.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.neuroscience.2018.08.016" target="_blank" rel="noreferrer noopener">10.1016/j.neuroscience.2018.08.016</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).
*Axonopathy
*axons
*neurodegeneration
*neurofilament
*node of Ranvier
*superior colliculus
2018
Crish S D
Dengler-Crish C M
Department of Pharmaceutical Sciences
Meier J
NEOMED College of Pharmacy
Neuroscience
Plyler E S
Smith M A
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.neuroscience.2018.08.016" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.neuroscience.2018.08.016</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
104-118
Volume
390
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Nodes of Ranvier in Glaucoma.
Publisher
An entity responsible for making the resource available
Neuroscience
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-10
Subject
The topic of the resource
Female; Male; Animals; Mice; *axonopathy; *axons; *neurodegeneration; *neurofilament; *node of Ranvier; *superior colliculus; Axons/pathology; Action Potentials; Inbred C57BL; Transgenic; Cytoskeleton/pathology; Glaucoma/metabolism/pathology/*physiopathology; Optic Nerve/metabolism/pathology; Ranvier's Nodes/*physiology/ultrastructure; Visual Pathways/metabolism/*physiopathology/ultrastructure; Voltage-Gated Sodium Channels/metabolism
Creator
An entity primarily responsible for making the resource
Smith M A; Plyler E S; Dengler-Crish Christine M; Meier J; Crish S D
Description
An account of the resource
Retinal ganglion cell axons of the DBA/2J mouse model of glaucoma, a model characterized by extensive neuroinflammation, preserve synaptic contacts with their subcortical targets for a time after onset of anterograde axonal transport deficits, axon terminal hypertrophy, and cytoskeletal alterations. Though retrograde axonal transport is still evident in these axons, it is unknown if they retain their ability to transmit visual information to the brain. Using a combination of in vivo multiunit electrophysiology, neuronal tract tracing, multichannel immunofluorescence, and transmission electron microscopy, we report that eye-brain signaling deficits precede transport loss and axonal degeneration in the DBA/2J retinal projection. These deficits are accompanied by node of Ranvier pathology - consisting of increased node length and redistribution of the voltage-gated sodium channel Nav1.6 that parallel changes seen early in multiple sclerosis (MS) axonopathy. Further, with age, axon caliber and neurofilament density increase without corresponding changes in myelin thickness. In contrast to these findings in DBA/2J mice, node pathologies were not observed in the induced microbead occlusion model of glaucoma - a model that lacks pre-existing inflammation. After one week of systemic treatment with fingolimod, an immunosuppressant therapy for relapsing-remitting MS, DBA/2J mice showed a substantial reduction in node pathology and mild effects on axon morphology. These data suggest that neurophysiological deficits in the DBA/2J may be due to defects in intact axons and targeting node pathology may be a promising intervention for some types of glaucoma.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.neuroscience.2018.08.016" target="_blank" rel="noreferrer noopener">10.1016/j.neuroscience.2018.08.016</a>
*Axonopathy
*axons
*neurodegeneration
*neurofilament
*node of Ranvier
*superior colliculus
2018
Action Potentials
Animals
Axons/pathology
Crish S D
Cytoskeleton/pathology
Dengler-Crish Christine M
Department of Pharmaceutical Sciences
Female
Glaucoma/metabolism/pathology/*physiopathology
Inbred C57BL
Male
Meier J
Mice
NEOMED College of Pharmacy
Neuroscience
Optic Nerve/metabolism/pathology
Plyler E S
Ranvier's Nodes/*physiology/ultrastructure
Smith M A
Transgenic
Visual Pathways/metabolism/*physiopathology/ultrastructure
Voltage-Gated Sodium Channels/metabolism