Fibiger H C, Phillips A G
Brain Res. 1976 Oct 29;116(1):23-33. doi: 10.1016/0006-8993(76)90246-8.
Stimulation of the zona compacta of the substantia nigra (SNC) has been reported to impair the long-term retention of a passive avoidance step-down task. In the present experiments it was observed that previous ipsilateral lesions of the dopaminergic nigro-neostriatal bundle (NSB) with 6-hydroxydopamine blocked the stimulation-induced memory deficit. Unilateral or bilateral lesions of the dopaminergic NSB did not by themselves disrupt acquisition or retention of the passive avoidance task. In addition, the memory deficit observed after electrical stimulation of the caudate-putamen was not reduced by ipsilateral NSB lesions. These results indicate that the retention deficit produced by stimulation of the SNC was mediated by the dopaminergic NSB. However, in view of the fact that lesions of this projection did not affect acquisition or retention of the step-down task, it is suggested that this system is not critically involved in learning and memory. Rather, it is hypothesized that stimulation of the SNC results in an excess release of dopamine in the caudateputamen which interferes with neurochemical and neurophysiological events in this structure which are important substrates for long-term memory.
据报道，刺激黑质致密部（SNC）会损害被动回避跳台任务的长期记忆。在本实验中观察到，先前用6-羟基多巴胺对多巴胺能黑质-新纹状体束（NSB）进行同侧损伤可阻断刺激诱导的记忆缺陷。多巴胺能NSB的单侧或双侧损伤本身并不会破坏被动回避任务的习得或记忆保持。此外，尾状核-壳核电刺激后观察到的记忆缺陷并未因同侧NSB损伤而减轻。这些结果表明，刺激SNC产生的记忆保持缺陷是由多巴胺能NSB介导的。然而，鉴于该投射的损伤并不影响跳台任务的习得或记忆保持，提示该系统并非学习和记忆的关键参与者。相反，据推测，刺激SNC会导致尾状核-壳核中多巴胺过度释放，从而干扰该结构中对长期记忆至关重要的神经化学和神经生理事件。
