N-cadherin is regulated by gonadal steroids in adult sexually dimorphic spinal motoneurons

Douglas A. Monks, Spiro Getsios, Colin D. MacCalman, Neil V. Watson*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

15 Scopus citations

Abstract

Gonadal steroids influence the morphology and function of neurons in the adult spinal cord through cellular and molecular mechanisms that are largely unknown. The cadherins are cell adhesion molecules that participate in the formation and organization of the CNS during embryonic development, and recent evidence suggests that the cadherins continue to regulate neural structure and function in adulthood. Using degenerate oligonucleotides coding conserved regions of the catenin-binding domain of classical cadherins in a RT-PCR cloning strategy, we identified several cadherin subtypes, the most frequently cloned being N-, E-, and R-cadherin, suggesting that these are the major classical cadherin subtypes present in the adult male rat lumbosacral spinal cord. We then examined cadherin expression levels of these cadherin subtypes under steroid conditions known to induce plastic changes in spinal motoneurons. Semiquantitative PCR revealed that mRNA levels of N-cadherin, but not E-cadherin or R-cadherin, are elevated in castrated rats treated with testosterone, 17β-estradiol, or dihydrotestosterone relative to castrate rats not treated with steroids. Immunolocalization of N-cadherin revealed that steroid treatment increased N-cadherin expression levels in functionally related neural populations whose morphology and function are regulated by steroids. These results suggest a role for N-cadherin in steroid-induced neuroplastic change in the adult lumbar spinal cord.

Original languageEnglish (US)
Pages (from-to)255-264
Number of pages10
JournalJournal of Neurobiology
Volume47
Issue number4
DOIs
StatePublished - Jun 15 2001

Keywords

  • Androgens
  • Cell adhesion
  • Estrogens
  • Neuronal
  • Plasticity
  • Spinal cord

ASJC Scopus subject areas

  • Neuroscience(all)

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