Dokla C P, Thal L J
Neurology Service, San Diego Veterans Administration Medical Center, California 92161.
Behav Neurosci. 1988 Dec;102(6):861-71.
The effect of bilateral nucleus basalis magnocellularis (nBM) lesions on performance in the Morris water task was examined in the rat, and the ability of anticholinesterase inhibitors to reverse the behavioral deficit was evaluated. Lesions of nBM resulted in a prolongation of escape latency. A spatial probe trial revealed that animals with sham lesions swam a greater percentage of the distance in the platform quadrant; this finding was abolished by nBM lesions. Lesions of nBM produced a nonsignificant increase in both open-field activity and activity-box scores. In Experiment 1, administration of 0.32 mg/kg physostigmine on Day 3 only resulted in a decrease in escape latency. In Experiment 2, in which cholinesterase inhibitors were administered daily for 5 days, 0.32 mg/kg but not low-dose physostigmine or two substituted N,N-alkyl phenyl carbamate cholinesterase inhibitors (RA-6 and RA-7) again improved escape latency on Day 3. Thus it was concluded that nBM lesions impair behavior on the Morris water task and physostigmine shortens escape latency.
研究了大鼠双侧大细胞基底核（nBM）损伤对其在莫里斯水迷宫任务中表现的影响，并评估了抗胆碱酯酶抑制剂逆转行为缺陷的能力。nBM损伤导致逃避潜伏期延长。空间探索试验显示，假损伤动物在平台象限游动的距离占比更大；nBM损伤消除了这一发现。nBM损伤使旷场活动和活动箱得分均有不显著的增加。在实验1中，仅在第3天给予0.32mg/kg毒扁豆碱可使逃避潜伏期缩短。在实验2中，每天给予胆碱酯酶抑制剂，持续5天，0.32mg/kg剂量的药物可改善第3天的逃避潜伏期，但低剂量毒扁豆碱或两种取代的N，N-烷基苯基氨基甲酸酯类胆碱酯酶抑制剂（RA-6和RA-7）则无此作用。因此得出结论，nBM损伤会损害大鼠在莫里斯水迷宫任务中的行为，而毒扁豆碱可缩短逃避潜伏期。
