Expression of Full-Length trkB Receptors by Reactive Astrocytes after Chronic CNS Injury

Growth factors, including members of the neurotrophin family, are expressed by neuronal and glial elements following injury to the CNS. In order to assess the capacity for glial cells to respond to neurotrophins at sites of chronic injury, full-length trkB receptors were localized following implanta...

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Bibliographic Details
Published in:Experimental neurology 1997-12, Vol.148 (2), p.558-567
Main Authors: McKeon, Robert J., Silver, Jerry, Large, Thomas H.
Format: Article
Language:English
Subjects:
Animals
Animals, Newborn
astrocyte
Astrocytes - cytology
Astrocytes - metabolism
Astrocytes - pathology
Biological and medical sciences
Brain Injuries - metabolism
Brain Injuries - pathology
Cells, Cultured
Cerebral Cortex - metabolism
Cerebral Cortex - pathology
CNS injury
Collodion
In Situ Hybridization
Injuries of the nervous system and the skull. Diseases due to physical agents
Medical sciences
microglia
Nerve Regeneration
neurotrophin
neurotrophin receptor
Rats
Rats, Sprague-Dawley
Receptor Protein-Tyrosine Kinases - biosynthesis
Receptor, Ciliary Neurotrophic Factor
Receptors, Nerve Growth Factor - biosynthesis
regeneration
Traumas. Diseases due to physical agents
trk
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Summary:Growth factors, including members of the neurotrophin family, are expressed by neuronal and glial elements following injury to the CNS. In order to assess the capacity for glial cells to respond to neurotrophins at sites of chronic injury, full-length trkB receptors were localized following implantation of a nitrocellulose filter into the cerebral cortex for 30 days. Northern analysis demonstrated that filter implants contained cells expressing transcripts for full-length and truncated trkB receptors, in contrast to the predominant expression of truncated trkB receptors by cultured astrocytes.In situhybridization and immunohistochemistry using probes to the trkB kinase domain colocalized full-length receptors with GFAP-immunopositive reactive astrocytes adjacent to and within the filter implant. In contrast, OX-42-immunopositive microglia/macrophages were not stained for full-length trkB. These data indicate that reactive astrocytes can express functional trkB receptors following a chronic insult to the cerebral cortex and support the hypothesis that neurotrophins may regulate astrocytic responses to injury.
ISSN:0014-4886
1090-2430
DOI:10.1006/exnr.1997.6698