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Y Tsumamoto, K Yamashita, K Okada, T Kurokawa, H Yamashita, HK Mishima; Regulation of BDNF and Its Receptor TrkB in Retina of Normal Aged Mice and Senescence-accelerated Mice . Invest. Ophthalmol. Vis. Sci. 2002;43(13):323.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: In normal-tension glaucoma patients, retinal ganglion cells (RGCs) undergo cell death, even though the intraocular pressure (IOP) is within normal range. Older patients tend to suffer from normal-tension glaucoma more frequently than younger patients. We addressed to examine if senescence may decrease the expression levels of tissue brain-derived neurotrophic factor (BDNF) and its receptor TrkB which are thought to support the survival of RGCs. Methods:In order to investigate the effects of senescence on the expression level of tissue BDNF and TrkB, we examined the retina of normal ICR mice and senescence-accelerated mice (SAM). The expression of BDNF and TrkB was observed immunohistochemically in retinas of female ICR (normal) mice at the age of 2 weeks, 1, 4, 12 and 15 months, and of SAM mice (substrain P8, SAM-P8 and substrain r1, SAM-r1) at the age of 1, 4, 12 months. Results:Histological observation revealed that there was no significant difference in the retinas among ICR mice and SAM strains. The excavation of the optic nerve head due to high IOP was not observed, suggesting that the IOPs were within normal range in all mice. In ICR mice retina, BDNF and TrkB were expressed in nerve fiber layer and inner plexiform layer in all ages examined. In SAM strains, the expression levels of BDNF and TrkB decreased significantly as the mice became older. Conclusion:Our findings suggest that senescence-acceleration causes the reduction of BDNF and TrkB expression. Low BDNF and TrkB are closely related with the death of RGC. Taken together, the RGC death independent from high IOP might be caused by the accelerated senescence.
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