Meguro K, Yamaguchi S, Arai H, Nakagawa T, Doi C, Yamada M, Ikarashi Y, Maruyama Y, Sasaki H
Department of Geriatric Medicine, Tohoku University, School of Medicine, Sendai, Japan.
Pharmacol Biochem Behav. 1994 Nov;49(3):769-72. doi: 10.1016/0091-3057(94)90100-7.
Senescence-accelerated mice (SAM), a murine model of age-related deterioration in learning ability, were studied as to the acetylcholine (ACh) contents in the brain tissues and the effect of nicotine administration. We found that the ACh content of SAM-P/8 (accelerated senescence-prone) mice was lower than that of SAM-R/1 (accelerated senescence-resistant) mice in the midbrain thalamus and the hypothalamus. In addition, an IP administration of nicotine was found to improve learning ability of SAM-P/8 as shown by performance of a passive avoidance task. Nicotine may potentiate cognitive function in SAM-P/8.
衰老加速小鼠（SAM）是一种与年龄相关的学习能力衰退的小鼠模型，本研究针对其脑组织中的乙酰胆碱（ACh）含量以及尼古丁给药的影响展开。我们发现，在中脑丘脑和下丘脑中，SAM-P/8（易加速衰老）小鼠的ACh含量低于SAM-R/1（抗加速衰老）小鼠。此外，如被动回避任务表现所示，腹腔注射尼古丁可改善SAM-P/8小鼠的学习能力。尼古丁可能增强SAM-P/8小鼠的认知功能。
