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中枢去甲肾上腺素能投射的部分破坏会增加蓝斑核细胞的放电频率。

Subtotal destruction of central noradrenergic projections increases the firing rate of locus coeruleus cells.

作者信息

Chiodo L A, Acheson A L, Zigmond M J, Stricker E M

出版信息

Brain Res. 1983 Mar 28;264(1):123-6. doi: 10.1016/0006-8993(83)91128-9.

Abstract

The intraventricular administration of 6-hydroxydopamine was used to destroy 80-90% of the noradrenergic terminals in the forebrain of male rats with little apparent damage to the cells of origin in locus-coeruleus. Both 36 h and 21 days later the basal firing rate of these cells was elevated 4-fold above control levels. Moreover, microiontophoretic application of norepinephrine was significantly less effective in inhibiting the spontaneous activity of locus coeruleus cells in these rats relative to control animals. The increased firing may represent a compensatory response to the injury, leading to increased transmitter release release from terminals spared by the lesion.

摘要

通过脑室内注射6-羟基多巴胺来破坏雄性大鼠前脑中80-90%的去甲肾上腺素能终末,而蓝斑中的起源细胞几乎没有明显损伤。在36小时和21天后,这些细胞的基础放电频率均比对照水平升高了4倍。此外,相对于对照动物,在这些大鼠中通过微离子电泳施加去甲肾上腺素对抑制蓝斑细胞的自发活动的效果明显较差。放电增加可能代表对损伤的一种代偿反应,导致由损伤 spared的终末释放的递质增加。 (注:这里“spared”原文可能有误,推测是“spared”,暂按此翻译,可能影响整体理解准确性)

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