Molecular Biological Study on Mechanism of Neuronal Cell Death and Establishment of New Therapy in Glaucoma

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Cell death has been thought to be induced by glutamate that stimulates the N-methyl-d-aspatate (NMDA) receptor present on retinal ganglion cells and on cells in the inner nuclear layer. Knock out mice were used to elucidate the role of the NR2A and NR2B subunit of the NMDA receptor. Wild type and NR2A and NR2B subunit knock out mice were used. Transient retinal ischemia was induced by raising intraocular pressure (IOP) to 120mmHg. In the Wild type mice, all the retinal ganglion cells were lost after 14 days. The number of cells in the inner nuclear layer was decreased. The thickness of the inner plexiform layer was reduced. By contrast, the retina appeared to be normal, unaffected by the insult in the NR2A subunit knockout mice. While the NR2B subunit knock out mice also showed the same tendency. These results suggest that the subunit may have a direct role in the retinal cell death induced by ischemia-reperfusion.We quantifies the level of brain-derived neurotrophic factor (BDNF) in the retina of experimental ocular hypertension model rat. To induce unilateral IOP elevation, we used a model developed by Ueda et al. (1998). Fellow eyes were served as control. IOP was measured by pneumatonometer. After the duration of IOP elevation above 22 mmHg for 1, 2, 4 and 12 weeks, retinas were dissected out from both experimental and control eyes and used as samples. To quantify BDNF protein level, we used enzyme-linked immunosorbant assay. Retinal BDNF levels of hypertensive eye compared to control after 1, 2, 4 and 12 weeks of IOP elevation were 277%, 102%, 59% and 24%, respectively. This study clarifies that BDNF levels were dramatically altered in the retina of experimental ocular hypertension model rat.