Anderson C D, Mair R G, Langlais P J, McEntee W J
Behav Brain Res. 1986 Jul;21(1):21-7. doi: 10.1016/0166-4328(86)90056-2.
Cortical norepinephrine, dopamine and 3,4-dihydroxyphenylacetic acid were reduced by injection of 6-hydroxydopamine (6-OHDA) jointly into the cisterna magna and the dorsal noradrenergic bundle. On subsequent behavioral testing, deficits were observed for spatial delayed alternation learning, but not for active or passive avoidance. Treatment with clonidine resulted in a significant improvement in spatial delayed alteration for experimental as compared to control animals. Injections of 6-OHDA into the cisterna magna alone had no significant effect on brain chemistry or behavioral measures. These results are similar to previous observations following a bout of thiamine deficiency, in which cortical catecholamines were depleted in animals that had exhibited deficits for spatial delayed alternation learning. We argue that the cortical catecholamine deficits observed in post-thiamine-deficient animals are sufficient to account for the delayed alternation deficits observed in this animal model of Korsakoff's psychosis.
通过将6-羟基多巴胺（6-OHDA）联合注入小脑延髓池和背侧去甲肾上腺素能束，可使皮质去甲肾上腺素、多巴胺和3,4-二羟基苯乙酸减少。在随后的行为测试中，观察到空间延迟交替学习存在缺陷，但主动或被动回避学习无缺陷。与对照动物相比，可乐定治疗使实验动物的空间延迟交替学习有显著改善。单独向小脑延髓池注射6-OHDA对脑化学或行为指标无显著影响。这些结果与先前硫胺素缺乏发作后的观察结果相似，在硫胺素缺乏发作后，表现出空间延迟交替学习缺陷的动物皮质儿茶酚胺会减少。我们认为，在硫胺素缺乏后动物中观察到的皮质儿茶酚胺缺乏足以解释在科尔萨科夫精神病这个动物模型中观察到的延迟交替缺陷。
