Expression of full-length trkB receptors by reactive astrocytes after chronic CNS injury

Exp Neurol. 1997 Dec;148(2):558-67. doi: 10.1006/exnr.1997.6698.

Abstract

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 situ hybridization 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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Animals, Newborn
  • Astrocytes / cytology
  • Astrocytes / metabolism*
  • Astrocytes / pathology
  • Brain Injuries / metabolism*
  • Brain Injuries / pathology
  • Cells, Cultured
  • Cerebral Cortex / metabolism*
  • Cerebral Cortex / pathology
  • Collodion
  • In Situ Hybridization
  • Nerve Regeneration
  • Rats
  • Rats, Sprague-Dawley
  • Receptor Protein-Tyrosine Kinases / biosynthesis*
  • Receptor, Ciliary Neurotrophic Factor
  • Receptors, Nerve Growth Factor / biosynthesis*

Substances

  • Receptor, Ciliary Neurotrophic Factor
  • Receptors, Nerve Growth Factor
  • Collodion
  • Receptor Protein-Tyrosine Kinases