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电休克而非抗抑郁药物可增加大鼠脑中α1-肾上腺素能受体结合位点。

Electroconvulsive shock but not antidepressant drugs increases alpha 1-adrenoceptor binding sites in rat brain.

作者信息

Stockmeier C A, McLeskey S W, Blendy J A, Armstrong N R, Kellar K J

机构信息

Department of Pharmacology, Georgetown University School of Medicine, Washington, D.C. 20007.

出版信息

Eur J Pharmacol. 1987 Jul 23;139(3):259-66. doi: 10.1016/0014-2999(87)90582-6.

Abstract

Treatment of rats with electroconvulsive shock once daily for 10-12 days increased the density of alpha 1-adrenoceptors labeled by [3H]prazosin in homogenates of frontal cerebral cortex. A single treatment did not affect [3H]prazosin binding. Repeated treatment with electroconvulsive shock did not appear to affect alpha 1-adrenoceptor binding in the hippocampus or hypothalamus. Treatment of rats with reserpine also increased [3H]prazosin binding in the frontal cortex. In contrast to electroconvulsive shock, three weeks administration of tricyclic antidepressant drugs, monoamine oxidase inhibitors, or atypical antidepressant drugs did not significantly affect [3H]prazosin binding sites in the frontal cortex. The affinities of antidepressant drugs for alpha 1-adrenoceptors ranged from about 50 nM for tricyclic and atypical antidepressants to about 100 microM for monoamine oxidase inhibitors. The high affinities of the tricyclic and atypical antidepressant drugs for alpha 1-adrenoceptors could contribute to clinical differences between these classes of drugs and monoamine oxidase inhibitors. Furthermore, the electroconvulsive shock-induced increase in alpha 1-adrenoceptors could contribute to differences in clinical effects between this treatment and antidepressant drugs.

摘要

每天对大鼠进行一次电惊厥休克治疗,持续10 - 12天,可增加额叶大脑皮质匀浆中由[3H]哌唑嗪标记的α1 - 肾上腺素能受体的密度。单次治疗不影响[3H]哌唑嗪结合。重复进行电惊厥休克治疗似乎不影响海马体或下丘脑的α1 - 肾上腺素能受体结合。用利血平治疗大鼠也会增加额叶皮质中[3H]哌唑嗪的结合。与电惊厥休克不同,三环类抗抑郁药、单胺氧化酶抑制剂或非典型抗抑郁药连续给药三周对额叶皮质中[3H]哌唑嗪结合位点没有显著影响。抗抑郁药对α1 - 肾上腺素能受体的亲和力范围从三环类和非典型抗抑郁药的约50 nM到单胺氧化酶抑制剂的约100 μM。三环类和非典型抗抑郁药对α1 - 肾上腺素能受体的高亲和力可能导致这些药物类别与单胺氧化酶抑制剂之间的临床差异。此外,电惊厥休克诱导的α1 - 肾上腺素能受体增加可能导致这种治疗与抗抑郁药在临床效果上的差异。

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