正常眼圧縁内障モデルマウスにおける視神経伸長を促す薬物とそのメカニズム

• Published in: 日本薬理学会年会要旨集 p. 3-B-SS13-2
• Main Authors: 渋江, 省吾, 東田, 千尋
• Format: Journal Article
• Language: Japanese
• Published: 公益社団法人 日本薬理学会 2022
• Subjects: axon; retina; visual cortex
• ISSN: 2435-4953
• DOI: 10.1254/jpssuppl.96.0_3-B-SS13-2

Glaucoma is a major cause of irreversible blindness worldwide, and is evoked by degenerationand loss of retinal ganglion cells (RGC).  Current drug treatments are focused on lowering intraocular pressure, which don't accomplish vision recovery. Our laboratory previously found axonal regeneration activity of Drug A (name is closed due to the patent). Therefore, this study aimed to investigate effects of Drug A on optic nerve growth in an optic nerve crush model.Based on our previous data showing that intravitreal injection of Drug A increased optic nerve density in the optic nerve crush model, this study aims to investigate oral treatability and potency of Drug A.At first, we evaluated brain penetration of Drug A after p.o. administration. Drug A was detected in the retina, the optic nerve and whole brain at least 6h after p.o. administration.Immediately after optic nerve crushing, Drug A or vehicle solution was administered orally for 3 weeks. Intraocular pressure measurements and a behavioral vision test were conducted on the day of sacrificing. After that, the retina, optic nerves and brain were dissected and served for histochemical evaluation. The number of retinal ganglion cells and optic nerve termination to the lateral geniculate nucleus were increased by Drug A. Drug A treatment to primary cultured RGC for 4 days significantly enhanced axonal length. The mechanism of Drug A for axonal growth of RGC is under investigation.