Aaltonen M, Riekkinen P, Sirviö J, Riekkinen P
Department of Neurology, University of Kuopio, Finland.
Pharmacol Biochem Behav. 1991 Jul;39(3):563-7. doi: 10.1016/0091-3057(91)90128-o.
Bilateral quisqualic acid nucleus basalis (NB) lesions impaired passive avoidance (PA) retention. NB lesions did not impair acquisition performance (stable platform location) in the water maze (WM). However, NB-lesioned rats were impaired in learning the new location of the escape platform in WM. Pretraining injections of tacridine (an anticholinesterase, THA) at 3 mg/kg, but not at 1 mg/kg, slightly improved PA retention performance in NB-lesioned rats. THA (1 or 3 mg/kg) did not alleviate NB lesion-induced WM defect. The results further suggest that loss of NB neurons impair PA acquisition and relearning of the new platform location in WM, and that cholinergic neuron loss may be at least partially involved in the NB lesion-induced performance defect.
双侧基底核喹啉酸损伤损害了被动回避记忆。基底核损伤并未损害水迷宫中获取任务的表现（平台稳定位置）。然而，基底核损伤的大鼠在学习水迷宫中逃生平台的新位置时受到损害。在基底核损伤的大鼠中，预训练注射3mg/kg的他克林（一种抗胆碱酯酶，THA）可轻微改善被动回避记忆表现，但1mg/kg则无此效果。THA（1或3mg/kg）并未减轻基底核损伤引起的水迷宫缺陷。结果进一步表明，基底核神经元的丧失损害了被动回避记忆的获取以及水迷宫中新平台位置的重新学习，并且胆碱能神经元的丧失可能至少部分参与了基底核损伤引起的行为缺陷。
