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Dynorphin A-(1-13) and (2-13) improve β-amyloid peptide-induced amnesia in mice

Hiramatsu, Masayuki1,2; Inoue, Kaori1; Kameyama, Tsutomu1


The anti-amnesic effects of dynorphins on β-amyloid peptide-(25–35)-induced impairment of learning and/or memory in mice were investigated using a Y-maze task and a passive avoidance test. Administration of β-amyloid peptide-(25–35) (βAP(25–35); 8.2 nmol, i.c.v.) 7 and 14 days before behavioral tests induced a decrease in both alternation behavior and latency in passive avoidance tests. Dynorphin A-(1–13) and A-(2–13) (0.5 and/or 1.5 nmol, i.c.v.) 30 min before behavioral tests improved the β-amyloid peptide-(25–35)-induced impairment of alternation performance and shortened the step-down latency. Nor-binaltorphimine (4.9 nmol, i.c.v.) partially blocked the effects of dynorphin A-(1–13), but not A-(2–13). These results indicate that dynorphin A-(1–13) and A-(2–13) improve amnesia induced by βAP-(25–35) via not only kappa opioid receptors, but also by non-opioid mechanisms.

1Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Meijo University, 150 Yagotoyama, Tenpaku-ku, Nagoya 468-8503, Japan

2Corresponding Author: Masayuki Hiramatsu

Acknowledgements: We express our gratitude to Dr T. Maurice (INSERM, France) for his excellent help. This study was supported in part by grants from the Japan Smoking Research Foundation, INSERM/JSPS Joint Research Project, and by Grants-in-Aids for Scientific Research (High-Tech Research Center Project) from the Ministry of Education, Science, Sports and Culture, Japan.

Received 18 August 1999; accepted 1 December 1999

© 2000 Lippincott Williams & Wilkins, Inc.