Review ArticleReduction of vesicular acetylcholine transporter in β-amyloid protein-infused rats with memory impairmentIKEDA, E.1*; SHIBA, K.2; MORI, H.2; ICHIKAWA, A.3; SUMIYA, H.1; KUJI, I.1; TONAMI, N.1Author Information 1Department of Nuclear Medicine, Kanazawa University School of Medicine, Kanazawa, 2Radioisotope Centre, Kanazawa University, Kanazawa and 3Department of Nuclear Medicine, Gunma University School of Medicine, Maebashi, Japan *Address all correspondence to Eiji Ikeda, Department of Nuclear Medicine, Kanazawa University School of Medicine, 13-1 Takara-Machi, Kanazawa, 920-8640, Japan. Tel: +81-76-265-2333; fax: +81-76-234-4257. Received 18 January 2000, in revised form 12 June 2000 and accepted 23 June 2000 Nuclear Medicine Communications: October 2000 - Volume 21 - Issue 10 - p 933-937 Buy Abstract The aim of this study was to investigate spatial memory and quantitative acetylcholine transporter autoradiography using a high-sensitivity imaging plate system in rats treated with β-amyloid protein, a model of Alzheimer's disease. An eight-arm radial maze was used to evaluate spatial memory. The performance of the eight-arm radial maze task was impaired in β-amyloid protein-treated rats. In the parietal cortex, [3H]-vesamicol binding to the vesicular acetylcholine transporter was significantly lower in β-amyloid protein-treated rats than in vehicle-treated rats, and was significantly correlated with the mean number of correct selections in the maze task of the first 5 days in the post-operative state. These results indicate that the reduction in [3H]-vesamicol binding to vesicular acetylcholine transporter is related to memory impairment induced by β-amyloid protein. β-Amyloid protein-infused rats with spatial memory impairment may be useful for the development of new radiolabelled vesamicol analogues for the objective evaluation of Alzheimer's disease. © 2000 Lippincott Williams & Wilkins, Inc.