Histological Protection by Donepezil Against Neurodegeneration Induced by Ischemia-Reperfusion in the Rat Retina
-
- Sakamoto Kenji
- Department of Molecular Pharmacology, Kitasato University School of Pharmaceutical Sciences, Japan
-
- Ohki Kayo
- Department of Molecular Pharmacology, Kitasato University School of Pharmaceutical Sciences, Japan
-
- Saito Maki
- Department of Molecular Pharmacology, Kitasato University School of Pharmaceutical Sciences, Japan
-
- Nakahara Tsutomu
- Department of Molecular Pharmacology, Kitasato University School of Pharmaceutical Sciences, Japan
-
- Ishii Kunio
- Department of Molecular Pharmacology, Kitasato University School of Pharmaceutical Sciences, Japan
この論文をさがす
抄録
Although a blockade of acetylcholine esterase has been reported to suppress neuronal cell death induced by exogenous glutamate and β-amyloid, information is still limited regarding the neuroprotective effects of the acetylcholine esterase inhibitor donepezil. We histologically examined the effects of donepezil on neuronal injury induced by ischemia–reperfusion. Intravenous and intravitreous treatment with donepezil 15 min prior to ischemia dramatically reduced the retinal damage. The protective effect of donepezil in the ganglion cell layer was not affected by mecamylamine, a nicotinic acetylcholine-receptor antagonist, nor scopolamine, a muscarinic acetylcholine-receptor antagonist. The protective effect of donepezil in the inner plexiform layer was reduced not by mecamylamine, but by scopolamine. Neostigmine, a choline-esterase inhibitor, and pilocarpine, a muscarinic acetylcholine-receptor agonist, have protective effects in the inner plexiform layer and the inner nuclear layer. These results suggest that not only the activation of acetylcholine receptors but also a mechanism unrelated to acetylcholine-esterase inhibition contribute to the protective effect of donepezil on the ganglion cells in the ischemic–reperfused rat retina. Donepezil may be useful as a therapeutic drug against retinal diseases that cause neuronal cell death such as glaucoma with high intraocular pressure.
収録刊行物
-
- Journal of Pharmacological Sciences
-
Journal of Pharmacological Sciences 112 (3), 327-335, 2010
公益社団法人 日本薬理学会
- Tweet
詳細情報 詳細情報について
-
- CRID
- 1390282680155602176
-
- NII論文ID
- 10027744508
- 130000251727
-
- NII書誌ID
- AA11806667
-
- COI
- 1:CAS:528:DC%2BC3cXktFOgs7Y%3D
-
- ISSN
- 13478648
- 13478613
-
- NDL書誌ID
- 10606864
-
- PubMed
- 20197638
-
- 本文言語コード
- en
-
- データソース種別
-
- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
- KAKEN
-
- 抄録ライセンスフラグ
- 使用不可