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Protective effects of selegiline and desmethylselegiline against N-methyl--aspartate-induced rat retinal damage

Posted by on in 2003
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 European Journal of Pharmacology, Volume 458, Issues 1-2 , 1 January 2003, Pages 81-89
Kazue Takahata (a), Hiroshi Katsuki (b), Yutaka Kobayashi (a), Shizuko Muraoka (a), Fumio Yoneda (a), Toshiaki Kume (b), Satoshi Kashii (c), Yoshihito Honda (c) and Akinori Akaike (b)
(a) Institute of Research and Development, Fujimoto Pharmaceutical Corporation, 1-3-40 Nishiotsuka, Matsubara, Osaka 580-8503, Japan
(b) Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, Yoshida-Shimoadachi-cho, Sakyo, Kyoto 606-8501, Japan
(c) Department of Ophthalmology and Visual Sciences, Graduate School of Medicine, Kyoto University, Yoshida-Konoe-cho, Sakyo, Kyoto 606-8501, Japan
Received 20 June 2002; revised 5 November 2002; accepted 6 November 2002; Available online 2 December 2002.


Selegiline, a therapeutic agent of Parkinson's disease, and its metabolite, desmethylselegiline, were explored for their neuroprotective effects against N-methyl--aspartate (NMDA)-induced cell death in rat retina. Morphometric analysis of the retina revealed that an intravitreal injection of NMDA induced a significant decrease in cell density in the ganglion cell layer and in thickness of the inner plexiform layer, but not of other retinal layers such as the outer nuclear layer. Concurrent intravitreal injection of selegiline with NMDA did not show a significant protective effect, whereas co-injection of desmethylselegiline provided protection from NMDA-induced retinal damage. Parenteral administration (both single and consecutive dosing) of selegiline significantly prevented loss of ganglion cell layer cells. Counting of retinal ganglion cells by fluorescent tracer labeling confirmed that selegiline protected retinal ganglion cells from NMDA toxicity. The selegiline treatment did not produce a significant increase, though it tended to such as effect, in a brain-derived neurotrophic factor (BDNF) level in the retina, when compared with the NMDA-treated control group. These results indicate that parenteral treatment with selegiline rescues inner retinal cells from NMDA-induced neural damage, and that desmethylselegiline may contribute, in part, to the protective activities of selegiline. The neuroprotective effects exerted by selegiline may be attributed partially to a change in the retinal BDNF expression.

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