Whishaw I Q, O'Connor W T, Dunnett S B
Behav Brain Res. 1985 Sep-Oct;17(2):103-15. doi: 10.1016/0166-4328(85)90023-3.
Rats with ibotenic acid lesions of the nucleus basalis magnocellularis, the origin of the extrinsic cholinergic innervation of the cortex, were examined for changes in feeding, sensorimotor behaviour, nocturnal locomotor activity, and place navigation in the Morris swimming pool task, in comparison with control rats and rats receiving the muscarinic antagonist, atropine. The lesions produced acute feeding impairments, marked by weight loss and vigorous active rejection of food and water lasting 2-4 days, sensorimotor impairments in placing and orienting, and overnight hyperactivity. A similar hyperactivity was induced by atropine, lasting approximately 6 h following the injection. Rats with lesions or receiving atropine were similarly impaired in the acquisition of the spatial navigation task, they failed to reach control levels of efficiency even once they had acquired the task, and they showed small but significant retention impairments when pretrained in the absence of either treatment. The results are discussed in terms of the lesions producing a disruption of cortical cholinergic systems, with implications for the clinical disorder of senile dementia of the Alzheimer type, and in terms of possible associated disruption to non-cholinergic systems.
用鹅膏蕈氨酸损毁大鼠基底前脑大细胞部(皮质外源性胆碱能神经支配的起源部位),并与对照大鼠和接受毒蕈碱拮抗剂阿托品的大鼠进行比较,检测其在进食、感觉运动行为、夜间运动活动以及在莫里斯游泳池任务中的空间导航方面的变化。损毁导致急性进食障碍,表现为体重减轻以及持续2 - 4天的对食物和水的强烈主动拒斥,在放置和定向方面存在感觉运动障碍,以及夜间活动亢进。阿托品也诱发了类似的活动亢进,注射后持续约6小时。有损毁或接受阿托品的大鼠在空间导航任务的习得方面同样受损,即使在习得任务后也未能达到对照水平的效率,并且在未进行任何一种处理的情况下预先训练时,它们表现出虽小但显著的记忆保持障碍。本文从损毁导致皮质胆碱能系统破坏的角度进行了讨论,这对阿尔茨海默型老年痴呆的临床病症具有启示意义,同时也从可能对非胆碱能系统造成相关破坏的角度进行了讨论。