强啡肽A-（1-13）减轻大鼠基底前脑损伤诱导的失忆。

Dynorphin A-(1-13) attenuates basal forebrain-lesion-induced amnesia in rats.

作者信息

Ukai M, Kobayashi T, Kameyama T

机构信息

Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Meijo University, Nagoya, Japan.

出版信息

Brain Res. 1993 Oct 22;625(2):355-6. doi: 10.1016/0006-8993(93)91082-4.

DOI:10.1016/0006-8993(93)91082-4

PMID:7903901

Abstract

The effects of dynorphin A-(1-13), an endogenous kappa opioid agonist, on basal forebrain (BF)-lesion-induced amnesia in rats were investigated using step-through-type passive avoidance task. The BF was lesioned by injecting the cholinergic neurotoxin ibotenic acid (6 micrograms/side). The number of rats achieving the cut-off time (600 s) of step-through latency (STL) in BF-lesioned group significantly decreased as compared with that in sham-operated group. Dynorphin A-(1-13) (0.3 micrograms) significantly increased the number of rats achieving the cut-off time of STL in BF-lesioned rats. These results suggest that dynorphins play an improving role in the impairment of memory processes in BF-lesioned rats.

摘要

采用穿梭式被动回避任务，研究内源性κ阿片受体激动剂强啡肽A-（1-13）对大鼠基底前脑（BF）损伤所致失忆的影响。通过注射胆碱能神经毒素鹅膏蕈氨酸（6微克/侧）损伤BF。与假手术组相比，BF损伤组达到穿梭潜伏期（STL）截止时间（600秒）的大鼠数量显著减少。强啡肽A-（1-13）（0.3微克）显著增加了BF损伤大鼠中达到STL截止时间的大鼠数量。这些结果表明，强啡肽对BF损伤大鼠的记忆过程损伤具有改善作用。