Development and role of retinal glia in regeneration of ganglion cells following retinal injury

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Abstract

Aims/background - Recent observations have shown that the glial scar resulting from a surgical lesion of the immature retina differs from elsewhere in the central nervous system, in that it permits the through growth and reconnection of regenerating axons. This study ire the opossum examines in detail the development and reaction to injury of retinal glia at different developmental stages, and specifically examines the distribution of the gliosis related inhibitory molecule, chondroitin sulphate proteoglycan (CSPG), making comparisons with a control site of gliosis in the cerebral cortex. Methods - A linear silt was cut into the retina or cortex with a fine tungsten probe. After a variable time delay, immunocytochemistry of the resulting gliosis was employed to detect astrocytes with glial fibrillary acidic protein (GFAP), Muller cells with vimentin, and CSPG with CS-56 antibodies. GFAP was also used at different ages to examine the normal development of astrocytes in the retina of this species. Results - Astrocytes entered the retina 12 days after birth (P12), closely associated with blood vessels in the nerve fibre layer. In experiments at all ages studied, cellular continuity was re-established across the lesioned retina, which did not result in a significant astrocyte proliferation or CSPG expression. In contrast, cortical injury led to the development of a cystic cavity surrounded by astrocytes and CSPG. Muller cells expressed GFAP but not CSPG in the lesioned retina. Conclusion - Successful regrowth ganglion cells through a retinal lesion may be partly the result of the scarcity of astrocytes in the retina, which results in minimal gliosis, or of their apparent inability to express inhibitory molecules.

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APA

MacLaren, R. E. (1996). Development and role of retinal glia in regeneration of ganglion cells following retinal injury. British Journal of Ophthalmology, 80(5), 458–464. https://doi.org/10.1136/bjo.80.5.458

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