Mitchell J A, Channell S, Hall G
Behav Neurosci. 1985 Dec;99(6):1074-88. doi: 10.1037//0735-7044.99.6.1074.
Experiment 1 demonstrated that rats with caudate-putamen lesions show an impairment in the acquisition and reversal of a spatial maze task when compared with unoperated control subjects. Experiment 2 examined lever-press responding supported by a variable interval schedule in three groups of subjects: a group with caudate-putamen lesions, a group with lesions of the posterior cortex, and an unoperated control group. The presentation of a 0.5-s, response-contingent light correlated with reinforcement generated an elevated response rate in the two operated groups but tended to suppress responding in the control group, perhaps by overshadowing the response-reinforcer relation. Only the group with cortical lesions maintained the elevated rate when the light was uncorrelated with food delivery. Experiment 3 confirmed for these same subjects that caudate-putamen lesions produce a spatial learning deficit. No deficit was seen in the posterior cortex group. It is suggested that caudate-putamen lesions disrupt the mechanism underlying the response-reinforcer association upon which spatial maze learning and free operant responding in part depend.
实验1表明,与未做手术的对照动物相比,尾状核-壳核受损的大鼠在空间迷宫任务的习得和逆转方面表现出损伤。实验2在三组动物中检验了由可变间隔程序支持的杠杆按压反应:一组是尾状核-壳核受损的动物,一组是后皮质受损的动物,还有一组是未做手术的对照动物。呈现一个与强化相关的0.5秒的、依反应而定的光,在两个做手术的组中产生了提高的反应率,但在对照组中却倾向于抑制反应,这可能是因为掩盖了反应与强化物之间的关系。当光与食物投放不相关时,只有后皮质受损的组保持了提高的反应率。实验3对这些相同的动物证实,尾状核-壳核受损会导致空间学习缺陷。在后皮质组中未观察到缺陷。有人提出,尾状核-壳核受损会破坏反应与强化物关联的潜在机制,而空间迷宫学习和自由操作反应在一定程度上依赖于这一机制。