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Abstract #25756 Published in IGR 12-2
Glaucomatous optic nerve injury involves early astrocyte reactivity and late oligodendrocyte loss
Son JL; Soto I; Oglesby E; Lopez-Roca T; Pease ME; Quigley HA; Marsh-Armstrong NGLIA 2010; 58: 780-789
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.
N. Marsh-Armstrong. Hugo W. Moser Research Institute at Kennedy Krieger, 707 North Broadway, Baltimore, MD 21205, United States. marsh-armstrong@kennedykrieger.org
Classification:
11.8 Neuroprotection (Part of: 11 Medical treatment)
5.1 Rodent (Part of: 5 Experimental glaucoma; animal models)
3.6 Cellular biology (Part of: 3 Laboratory methods)