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

TitleGlaucomatous optic nerve injury involves early astrocyte reactivity and late oligodendrocyte loss.
Publication TypeJournal Article
Year of Publication2010
AuthorsSon JL, Soto I, Oglesby E, Lopez-Roca T, Pease ME, Quigley HA, Marsh-Armstrong N
JournalGlia
Volume58
Issue7
Pagination780-9
Date Published2010 May
Abstract

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.

DOI10.1177/0883073809350221
Alternate JournalGlia