Exp Neurobiol 2003; 12(2): 97-103
Published online December 31, 2003
© The Korean Society for Brain and Neural Sciences
Gye Sun Jeon1 and Sa Sun Cho1,2,*
1Department of Anatomy, Seoul National University College of Medicine, Seoul 110-799, Korea, 2Neuroscience Research Institute, MRC, Seoul National University, Seoul 110-799, Korea
Correspondence to: *To whom correspondence should be addressed.
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Quail retinae were stained immunocytochemically with monoclonal antibody QH1, a specific marker for quail microglia, at various times up to 6 mo after unilateral intraorbital optic nerve transection, which is known to induce degeneration of ganglion cell axons and perikarya in the retina. A few days after transection, activated microglia displaying an amoeboid shape and strong QH1-immunoreactivity began to appear in the inner part of the retina including the inner plexiform layer. The number of these amoeboid cells transiently increased, particularly in the ganglion cell and in the optic nerve fiber layers, where retrograde neuronal degeneration actively occurs, and returned to the normal value 6 mo post-transection. In addition, we observed that numerous QH1-labeled macrophages intimately adhered to the surfaces of the pecten and the optic disc, and subsequently radially oriented in the retina. Furthermore, some of these vitreal macrophages and retinal microglia were labeled with PCNA, indicated migration and proliferation around the optic disc. The results of this study, for the first time, describe the temporal and spatial aspects of microglial activation in the avascular retina, and suggest that the proliferation of microglia and the migration of macrophages, attributable to a massive increase of activated microglia at the lesion site during microglial activation, is a property shared by vascular and avascular central nervous system (CNS) tissue.
Keywords: Optic nerve transection, microglia, macrophages, proliferation, migration