Abstract
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 alternation 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.
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