Glutamate receptor-mediated retinal neuronal injury in experimental glaucoma.
- Author:
Zhong-Feng WANG
1
;
Xiong-Li YANG
2
Author Information
1. Institutes of Brain Science, Institute of Neurobiology, State Key Laboratory of Medical Neurobiology, Shanghai Key Laboratory of Visual Impairment and Restoration, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China. zfwang@fudan.edu.cn.
2. Institutes of Brain Science, Institute of Neurobiology, State Key Laboratory of Medical Neurobiology, Shanghai Key Laboratory of Visual Impairment and Restoration, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Disease Models, Animal;
Glaucoma;
Ocular Hypertension;
Receptors, Glutamate;
Retina;
Retinal Ganglion Cells
- From:
Acta Physiologica Sinica
2016;68(4):483-491
- CountryChina
- Language:Chinese
-
Abstract:
Glaucoma, the second leading cause of blindness, is a neurodegenerative disease characterized by optic nerve degeneration related to apoptotic death of retinal ganglion cells (RGCs). In the pathogenesis of RGC death following the onset of glaucoma, functional changes of glutamate receptors are commonly regarded as important risk factors. During the past several years, we have explored the mechanisms underlying RGC apoptosis and retinal Müller cell reactivation (gliosis) in a rat chronic ocular hypertension (COH) model. We demonstrated that elevated intraocular pressure in COH rats may induce changes of various signaling pathways, which are involved in RGC apoptosis by modulating glutamate NMDA and AMPA receptors. Moreover, we also demonstrated that over-activation of group I metabotropic glutamate receptors (mGluR I) by excessive extracellular glutamate in COH rats could contribute to Müller cell gliosis by suppressing Kir4.1 channels. In this review, incorporating our results, we discuss glutamate receptor- mediated RGC apoptosis and Müller cell gliosis in experimental glaucoma.
