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多巴胺耗竭性脑损伤大鼠中激活诱导的感觉运动功能恢复

Activation-induced restoration of sensorimotor functions in rats with dopamine-depleting brain lesions.

作者信息

Marshall J F, Levitan D, Stricker E M

出版信息

J Comp Physiol Psychol. 1976 Jun;90(6):536-46. doi: 10.1037/h0077230.

Abstract

Bilateral electrolytic lesions of the lateral hypothalamus or intraventricular 6-hydroxydopamine injections produced substantial depletions of striatal dopamine in rates. All animals with brain damage showed marked sensorimotor impairments. However, they began to move and respond appropriately to environmental stimuli when placed in a sink of water, in a shallow ice bath, or among a colony of cats or rats. A reversal of the sensorimotor dysfunctions was still apparent shortly after the animals were removed from each activating situation. However, the terapeutic effects dissipated rapidly, and by 4 hr after an exposure the rats responded as poorly as they had prior to activation. These findings are strikingly similar to the "paradoxical kinesia" seen in parkinsonism, a clinical disorder attributed to degeneration of central dopamine-containing neurons. Collectively, they suggest the importance of activation in maintaining responsiveness to senory stimuli in rats following dopamine-depleting brain lesions.

摘要

下丘脑外侧的双侧电解损伤或脑室内注射6-羟基多巴胺会使大鼠纹状体多巴胺大量耗竭。所有脑损伤的动物均表现出明显的感觉运动障碍。然而,当将它们置于水槽、浅冰浴中,或置于一群猫或大鼠中时,它们开始移动并对环境刺激做出适当反应。在将动物从每种激活情境中移出后不久,感觉运动功能障碍的逆转仍然明显。然而,治疗效果迅速消散,暴露后4小时,大鼠的反应与激活前一样差。这些发现与帕金森病中出现的“矛盾性运动障碍”惊人地相似,帕金森病是一种临床疾病,归因于中枢含多巴胺神经元的退化。总体而言,它们表明激活对于维持多巴胺耗竭性脑损伤后大鼠对感觉刺激的反应性很重要。

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