Glaucomatous optic nerve injury involves early astrocyte reactivity and late oligodendrocyte loss

Janice L. Son, Ileana Soto, Ericka Oglesby, Teresa Lopez-Roca, Mary E. Pease, Harry A. Quigley, Nicholas Marsh-Armstrong

Research output: Contribution to journalArticlepeer-review

85 Scopus citations


Glaucoma, a neurodegenerative disease affecting retinal ganglion cells (RGC), is a leading cause of blindness. Since gliosis is common in neurodegenerative disorders, it is important to describe the changes occurring in various glial populations in glaucoma animal models in relation to axon loss, as only changes that occur early are likely to be useful therapeutic targets. Here, we describe changes occurring in glia within the myelinated portion of the optic nerve (ON) in both DBA/2J mice and in a rat ocular hypertension model. In both glaucoma animal models, we found only a modest loss of oligodendrocytes that occurred after axons had already degenerated. In DBA/2J mice there was proliferation of oligodendrocyte precursor cells (OPCs) and new oligodendrocyte generation. Activation of microglia was detected only in highly degenerated DBA/2J ONs. In contrast, a large increase in astrocyte reactivity occurred early in both animal models. These results are consistent with astrocytes playing a prominent role in regulating axon loss in glaucoma.

Original languageEnglish (US)
Pages (from-to)780-789
Number of pages10
Issue number7
StatePublished - May 2010
Externally publishedYes

ASJC Scopus subject areas

  • Neurology
  • Cellular and Molecular Neuroscience


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