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通过损毁背侧去甲肾上腺素能束对大鼠脑α和β肾上腺素能受体群体的调节

Modulation of rat brain alpha- and beta-adrenergic receptor populations by lesion of the dorsal noradrenergic bundle.

作者信息

U'Prichard D C, Reisine T D, Mason S T, Fibiger H C, Yamamura H I

出版信息

Brain Res. 1980 Apr 7;187(1):143-54. doi: 10.1016/0006-8993(80)90500-4.

DOI:10.1016/0006-8993(80)90500-4
PMID:6244065
Abstract

Bilateral lesion of the ascending noradrenergic fibers in the dorsal bundle of adult Wistar rats with 4 micrograms 6-hydroxydopamine caused extensive depletion of norepinephrine in all forebrain areas, but led to a 54% increase in norepinephrine levels in the cerebellum. beta-Adrenergic receptor binding of [3H]dihydroalprenolol was significantly increased in all forebrain areas depleted of norepinephrine except hypothalamus. The increase in [3H]dihydroalprenolol binding was due to 62% and 34% increases in the number of beta-receptor sites in the frontal cerebral cortex and hippocampus respectively. Binding of [3H]WB-4101 to alpha 1-adrenergic receptors after dorsal bundle lesion was augmented generally to a lesser extent than beta-receptor binding, with significantly increased numbers of sites only in the frontal cortex (74%), thalamus (20%) and septum. Both alpha 1- and beta-receptor binding sites were reduced in number by 25-28% in the cerebellum of dorsal bundle-lesioned rats, whereas intraventricular administration of 6-hydroxydopamine to adult rats, which depletes norepinephrine in the cerebellum by 96%, increased cerebellar alpha 1- and beta-receptor binding by 33-40%. Binding of [3H]clonidine to forebrain alpha 2-adrenergic receptors was significantly elevated in the frontal cortex, but reduced in the amygdala and septum, after dorsal bundle lesion.

摘要

用4微克6-羟基多巴胺对成年Wistar大鼠背束中的去甲肾上腺素能上行纤维进行双侧损伤,导致所有前脑区域的去甲肾上腺素大量耗竭,但小脑去甲肾上腺素水平却升高了54%。除下丘脑外,在所有去甲肾上腺素耗竭的前脑区域,[3H]二氢阿普洛尔与β-肾上腺素能受体的结合显著增加。[3H]二氢阿普洛尔结合的增加分别是由于额叶皮质和海马体中β-受体位点数量增加了62%和34%。背束损伤后,[3H]WB-4101与α1-肾上腺素能受体的结合总体上比β-受体结合增加的程度要小,只有额叶皮质(74%)、丘脑(20%)和隔区的位点数量显著增加。在背束损伤大鼠的小脑中,α1-和β-受体结合位点的数量减少了25%-28%,而对成年大鼠脑室内注射6-羟基多巴胺,使小脑中去甲肾上腺素耗竭96%,却使小脑α1-和β-受体结合增加了33%-40%。背束损伤后,[3H]可乐定与前脑α2-肾上腺素能受体的结合在额叶皮质显著升高,但在杏仁核和隔区降低。

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