Environmental enhancement of growth factor-mediated oligodendrocyte precursor proliferation

Shenandoah Robinson, Robert Miller

Research output: Contribution to journalArticle

Abstract

The timing of oligodendrogenesis depends on the specific location within the central nervous system, suggesting the local environment influences oligodendrocyte precursor proliferation. Spinal cord and optic nerve oligodendrocyte precursors both proliferate in response to platelet-derived growth factor (PDGF). Here we show that neurotrophin-3 (NT-3) enhanced PDGF- induced proliferation of optic nerve oligodendrocyte precursors, and these cells were labeled by an anti-trkC antibody. By contrast, NT-3 did not enhance PDGF-induced proliferation of spinal cord oligodendrocyte precursors, and these cells were not labeled by an anti-trkC antibody. Furthermore, PDGF- induced oligodendrocyte precursor proliferation was greater in spinal cord than in optic nerve cultures. The difference in NT-3 response between spinal cord and optic nerve oligodendrocyte precursors appears cell intrinsic, while the enhanced PDGF-induced proliferation of spinal cord oligodendrocyte precursors appears environmentally regulated. The spinal cord PDGF proliferation-enhancing activity may provide a mechanism to allow temporal and spatial regulation of gliogenesis.

Original languageEnglish (US)
Pages (from-to)38-52
Number of pages15
JournalMolecular and Cellular Neurosciences
Volume8
Issue number1
DOIs
StatePublished - Jul 1996
Externally publishedYes

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Oligodendroglia
Platelet-Derived Growth Factor
Intercellular Signaling Peptides and Proteins
Spinal Cord
Optic Nerve
Neurotrophin 3
Spinal Nerves
Anti-Idiotypic Antibodies
Central Nervous System

ASJC Scopus subject areas

  • Molecular Biology
  • Cellular and Molecular Neuroscience
  • Developmental Neuroscience

Cite this

Environmental enhancement of growth factor-mediated oligodendrocyte precursor proliferation. / Robinson, Shenandoah; Miller, Robert.

In: Molecular and Cellular Neurosciences, Vol. 8, No. 1, 07.1996, p. 38-52.

Research output: Contribution to journalArticle

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