期刊
FRONTIERS IN NEUROSCIENCE
卷 11, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fnins.2017.00235
关键词
glaucoma; chronic ocular hypertension; acute ocular hypertension; axotomy; Brn3a retinal ganglion cells; melanopsin retinal ganglion cells; cone photoreceptors; retinal nerve fiber layer
资金
- Fundacion Seneca, Agencia de Ciencia y Tecnologia Region de Murcia [19881/GERM/15]
- Spanish Ministry of Economy and Competitiveness, Institute de Salud Carlos III, Fondo Europeo de Desarrollo Regional Una Manera de Hacer Europa [SAF2015-676/13-P, PI16/00380, RD16/0008/0026, P116/00031]
Glaucoma, one of the leading causes of blindness worldwide, affects primarily retinal ganglion cells (RGCs) and their axons. The pathophysiology of glaucoma is not fully understood, but it is currently believed that damage to RGC axons at the optic nerve head plays a major role. Rodent models to study glaucoma include those that mimic either ocular hypertension or optic nerve injury. Here we review the anatomical loss of the general population of RGCs (that express Brn3a; Brn3a(+)RGCs) and of the intrinsically photosensitive RGCs (that express melanopsin; m(+)RGCs) after chronic (LP-OHT) or acute (A-OHT) ocular hypertension and after complete intraorbital optic nerve transection (ONT) or crush (ONC). Our studies show that all of these insults trigger RGC death. Compared to wBrn3a(+)ERGCs, m(+)RGCs are more resilient to ONT, ONC, and A-OHT but not to LP-OHT. There are differences in the course of RGC loss both between these RGC types and among injuries. An important difference between the damage caused by ocular hypertension or optic nerve injury appears in the outer retina. Both axotomy and LP-OHT induce selective loss of RGCs but LP-OHT also induces a protracted loss of cone photoreceptors. This review outlines our current understanding of the anatomical changes occurring in rodent models of glaucoma and discusses the advantages of each one and their translational value.
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