摘要
目的 研究阿片受体拮抗剂纳洛酮对血管性痴呆大鼠空间学习记忆减退的防治作用。方法 采用持久性结扎双侧颈总动脉方法制备血管性痴呆模型 ,随机分为假手术组、模型组和预防治疗组。防治组于术后即连续 7天腹腔注射纳洛酮。 8周后用Morris水迷宫训练方法 ,比较假手术组 +生理盐水组、模型组 +生理盐水组与模型组 +纳洛酮防治组大鼠的空间学习记忆能力的差异 ,观察纳洛酮对血管性痴呆大鼠空间学习记忆减退的防治作用。结果 假手术组 +生理盐水组和模型组 +纳洛酮防治组与模型组 +生理盐水组的实验大鼠相比 ,其Morris水迷宫隐匿平台逃避潜伏期明显缩短 (P <0 .0 0 1 ) ,前两者无显著性差异 (P >0 .0 5) ;空间探索实验穿越平台次数明显增加 (P <0 .0 0 1 ) ,前两者无显著性差异 (P >0 .0 5)。可见平台实验逃避潜伏期三组间无显著性差异 (P >0 .0 5)。结论 纳洛酮对血管性痴呆大鼠空间学习记忆减退有明显防治作用。其机理可能是纳洛酮及阿片受体在脑缺血中起调控作用 。
Objective To study the preventive effects of naloxone, a general competitive opioid receptor antagonist, on spatial learning and memory deficits in rats with vascular dementia(VD). Methods The rats model of vascular dementia were made by permanent bilateral occlusion of both common carotid arteries (2 VO methods),the models were divided into three groups at random: sham operated group?VD group and naloxone preventive treatment group. The latter group successively received naloxone treatment(naloxone hydrochloride, 0.8.kg -1 i.p.) for 7 days after the operation immediately, while the former two groups were received equal volume saline injected intraperitoneally. All of the rats were trained in Morris Water Maze orderly for 5 days to find the escape latencies. Spatial learning and memory abilities were evaluated with a series of tasks to find a hidden platform in Morris Water Maze. Results The escape latencies in VD rats with NS treatment are significantly longer than that in sham operated rats with NS treatment and that in VD rats with naloxone preventive treatment(P<0.001), There is no significant difference VD rats with naloxone preventive treatment and sham operated rats with NS treatment regarding to the escape latencies(P>0.05);The times of passing through the platform were significantly increased(P<0.001),there is no significantly difference between the two former groups (P>0.05)?The latencies are no significantly difference among three groups in the visible platform task training (P>0.05). Conclusions The preventive effects of naloxone on spatial learning and memory deficits in rats with VD are significantly.Its mechanism may be naloxone and opioid receptors act on important functions in regulating and controlling cerebral ischemia;naloxone acts on protective function in cerebral ischemia leading to selective hippocampus neurones loss.
出处
《中国行为医学科学》
CAS
CSCD
2002年第6期606-608,共3页
Chinese Journal of Behavioral Medical Science
基金
广东省自然科学基金项目项目编号 0 0 0 82 5
