The upregulation of nerve growth factor receptors in reactive astrocytes of rat spinal cord during experimental autoimmune encephalomyelitis

Barbara Oderfeld-Nowak, Malgorzata Zaremba, Alessandra Micera, Luigi Aloe

Research output: Contribution to journalArticlepeer-review

Abstract

Using immunocytochemistry, we have examined the effect of experimental autoimmune encephalomyelitis (EAE) upon the expression of nerve growth factor (NGF) and its TrkA and p75 receptors in astroglia cells of the spinal cord of Lewis rats. We have found that, in normal spinal cord, astroglia of white matter expressed both NGF receptors while those in gray matter expressed only TrkA and no astroglia expressed NGF. During EAE, strong upregulation of TrkA in the astroglia of gray and white matter was found, particularly in a population of radially oriented astrocytes. An upregulation of p75 was noted in radial astroglia and, to some extent, also in the stellate astrocytes of white matter. In general, the upregulation of NGF receptor immunoreactivities in astroglia correlated with the strong intensification of glial fibrillary acidic protein immunocytochemistry, a prominent feature of EAE. No NGF immunoreactivity appeared in any astroglia cells during EAE. Our results suggest that, during EAE, astroglia of the spinal cord become particularly receptive to NGF, possibly as part of a mechanism enabling astroglial cells to respond to localized release of neurotrophins. Moreover, our data suggest that spinal cord astroglia cells may be a potential target for pharmacological manipulations in EAE.

Original languageEnglish
Pages (from-to)165-168
Number of pages4
JournalNeuroscience Letters
Volume308
Issue number3
DOIs
Publication statusPublished - Aug 10 2001

Keywords

  • Astrocytes
  • Experimental autoimmune encephalomyelitis
  • Radial astroglia
  • Spinal cord
  • TrkA and p75 receptors

ASJC Scopus subject areas

  • Neuroscience(all)

Fingerprint Dive into the research topics of 'The upregulation of nerve growth factor receptors in reactive astrocytes of rat spinal cord during experimental autoimmune encephalomyelitis'. Together they form a unique fingerprint.

Cite this