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6-羟基多巴胺诱导脊髓去甲肾上腺素耗竭的行为学效应。

Behavioural effects of 6-hydroxydopamine-induced depletion of spinal noradrenaline.

作者信息

Roberts D C, McCaughran J A, Fibiger H C

出版信息

Can J Physiol Pharmacol. 1979 Nov;57(11):1223-8. doi: 10.1139/y79-184.

Abstract

Bilateral injection of 6-hydroxydopamine (4 micrograms/2 microL) into the caudal medulla of rats reduced spinal noradrenaline (NA) to 6% of control values. No significant NA depletion was observed in the hippocampus, cortex, or cerebellum, and a small loss of NA was found in the hypothalamus. These lesions were found to elevate significantly threshold shock levels necessary to elicit jump responses, and they also abolished the reflexive alternating motor movements produced by decapitation. These data support the hypothesis that spinal NA mechanisms modulate reflexive motor movements. However, no significant effect of these lesions was found on either spontaneous or amphetamine-induced locomotor activity, suggesting that spinal NA does not play a significant role in these behaviours.

摘要

向大鼠延髓尾部双侧注射6-羟基多巴胺(4微克/2微升)可使脊髓去甲肾上腺素(NA)降至对照值的6%。在海马体、皮质或小脑中未观察到明显的NA耗竭,而下丘脑中有少量NA损失。发现这些损伤显著提高了引发跳跃反应所需的阈下休克水平,并且它们还消除了断头引起的反射性交替运动。这些数据支持脊髓NA机制调节反射性运动的假说。然而,未发现这些损伤对自发或苯丙胺诱导的运动活动有显著影响,这表明脊髓NA在这些行为中不发挥重要作用。

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