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/10.1007/s002210000630" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s002210000630</a>
Pages
219–227
Issue
2
Volume
137
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
Neuropathic pain in aged rats: behavioral responses and astrocytic activation.
Publisher
An entity responsible for making the resource available
Experimental brain research
Date
A point or period of time associated with an event in the lifecycle of the resource
2001
2001-03
Subject
The topic of the resource
Aging/*physiology; Animal; Animal/*physiology; Animals; Astrocytes/*metabolism; Behavior; Cell Count; Disease Models; Functional Laterality/physiology; Glial Fibrillary Acidic Protein/metabolism; Hyperalgesia/physiopathology; Immunohistochemistry; Inbred F344; Lumbar Vertebrae; Male; Nerve Crush/methods; Neuralgia/*metabolism/pathology/physiopathology; Pain Measurement; Peripheral Nervous System Diseases/*metabolism/pathology/physiopathology; Posterior Horn Cells/*metabolism; Rats; Thermosensing/physiology; Touch/physiology; Up-Regulation/*physiology
Creator
An entity primarily responsible for making the resource
Stuesse S L; Crisp T; McBurney D L; Schechter J B; Lovell J A; Cruce W L
Description
An account of the resource
We used the Bennett and Xie (1988) model of chronic neuropathic pain to study the effect of age on thermal and tactile sensitivity and on astrocytic activation in the dorsal horn of the spinal cord after nerve injury. Fischer 344 FBNF1 hybrid rats in three age groups, 4-6, 14-16, and 24-26 months, were studied. Rats were either unligated (day 0, control) or the left sciatic nerve was loosely ligated to cause a chronic constriction injury (CCI). CCI causes a neuropathic pain condition characterized by tactile allodynia and thermal hyperalgesia. Rats were behaviorally assessed for tactile and thermal sensitivity of their ligated and unligated hind paws up to 35 days postligation. Rats were sacrificed before or at various days postligation, and activated astrocytes were identified at the L4-L5 levels of their spinal cords by use of an antibody to glial fibrillary acid protein (GFAP). The number of GFAP-ir astrocytes in the dorsal horn of the spinal cord in the control, uninjured condition decreased with age (P \textless or = 0.001) but increased after CCI in all three age groups. After CCI, astrocytic activation in the cord was less robust in aged rats than in younger ones (P \textless or = 0.01). Not all the CCI rats displayed hyperalgesia to touch and to heat. Rats with an increased sensitivity to heat had increased levels of GFAP-ir in their cords; however, rats with decreased thermal sensitivity also displayed increased
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s002210000630" target="_blank" rel="noreferrer noopener">10.1007/s002210000630</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2001
Aging/*physiology
Animal
Animal/*physiology
Animals
Astrocytes/*metabolism
Behavior
Cell Count
Crisp T
Cruce W L
Department of Anatomy & Neurobiology
Disease Models
Experimental brain research
Functional Laterality/physiology
Glial Fibrillary Acidic Protein/metabolism
Hyperalgesia/physiopathology
Immunohistochemistry
Inbred F344
Lovell J A
Lumbar Vertebrae
Male
McBurney D L
NEOMED College of Medicine
Nerve Crush/methods
Neuralgia/*metabolism/pathology/physiopathology
Pain Measurement
Peripheral Nervous System Diseases/*metabolism/pathology/physiopathology
Posterior Horn Cells/*metabolism
Rats
Schechter J B
Stuesse S L
Thermosensing/physiology
Touch/physiology
Up-Regulation/*physiology
-
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.2012.10.069" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.neuroscience.2012.10.069</a>
Pages
55–70
Volume
229
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
Failure of axonal transport induces a spatially coincident increase in astrocyte BDNF prior to synapse loss in a central target.
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
2013
2013-01
Subject
The topic of the resource
Animal; Animals; Astrocytes/*metabolism; Axonal Transport/*physiology; Brain-Derived Neurotrophic Factor/*metabolism; Disease Models; Glaucoma/genetics/*metabolism; Messenger/genetics/metabolism; Mice; Optic Nerve Diseases/genetics/metabolism; Rats; Retinal Ganglion Cells/*metabolism; RNA; Superior Colliculi/metabolism; Synapses/*metabolism; Visual Pathways/metabolism
Creator
An entity primarily responsible for making the resource
Crish S D; Dapper J D; MacNamee S E; Balaram P; Sidorova T N; Lambert W S; Calkins D J
Description
An account of the resource
Failure of anterograde transport to distal targets in the brain is a common feature of neurodegenerative diseases. We have demonstrated in rodent models of glaucoma, the most common optic neuropathy, early loss of anterograde transport along the retinal ganglion cell (RGC) projection to the superior colliculus (SC) is retinotopic and followed by a period of persistence of RGC axon terminals and synapses through unknown molecular pathways. Here we use the DBA/2J mouse model of hereditary glaucoma and an acute rat model to demonstrate that retinotopically focal transport deficits in the SC are accompanied by a spatially coincident increase in brain-derived neurotrophic factor (BDNF), especially in hypertrophic astrocytes. These neurochemical changes occur prior to loss of RGC synapses in the DBA/2J SC. In contrast to BDNF protein, levels of Bdnf mRNA decreased with transport failure, even as mRNA encoding synaptic structures remained unchanged. In situ hybridization signal for Bdnf mRNA was the strongest in SC neurons, and labeling for the immature precursor pro-BDNF was very limited. Subcellular fractionation of SC indicated that membrane-bound BDNF decreased with age in the DBA/2J, while BDNF released from vesicles remained high. These results suggest that in response to diminished axonal function, activated astrocytes in the brain may sequester mature BDNF released from target neurons to counter stressors that otherwise would challenge survival of projection synapses.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.neuroscience.2012.10.069" target="_blank" rel="noreferrer noopener">10.1016/j.neuroscience.2012.10.069</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2013
Animal
Animals
Astrocytes/*metabolism
Axonal Transport/*physiology
Balaram P
Brain-Derived Neurotrophic Factor/*metabolism
Calkins D J
Crish S D
Dapper J D
Department of Pharmaceutical Sciences
Disease Models
Glaucoma/genetics/*metabolism
Lambert W S
MacNamee S E
Messenger/genetics/metabolism
Mice
NEOMED College of Pharmacy
Neuroscience
Optic Nerve Diseases/genetics/metabolism
Rats
Retinal Ganglion Cells/*metabolism
RNA
Sidorova T N
Superior Colliculi/metabolism
Synapses/*metabolism
Visual Pathways/metabolism