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非典型抗精神病药物急性给药后结节漏斗多巴胺神经元的激活。

Activation of tuberoinfundibular dopamine neurons following the acute administration of atypical antipsychotics.

作者信息

Gudelsky G A, Meltzer H Y

机构信息

Department of Psychiatry, Case Western Reserve University, Cleveland, Ohio.

出版信息

Neuropsychopharmacology. 1989 Mar;2(1):45-51. doi: 10.1016/0893-133x(89)90006-7.

Abstract

The activity of tuberoinfundibular dopamine neurons, as judged from dihydroxyphenylacetic acid (DOPAC) concentrations or the accumulation of dihydroxyphenylalanine (DOPA) in the median eminence after the inhibition of DOPA decarboxylase, was increased following the acute administration of the purported atypical antipsychotics clozapine, thioridazine, melperone, setoperone, and RMI 81582. In contrast, the activity of these hypothalamic dopamine neurons was not acutely altered by the typical antipsychotics haloperidol, chlorpromazine, fluphenazine, and cis-flupentixol or by SCH 23390. The acute stimulatory effect of the atypical antipsychotics on the activity of tuberoinfundibular dopamine neurons was effectively antagonized by the D1 agonist SKF 38393 but not by the D2 agonist quinpirole. The production of an acute activation of tuberoinfundibular dopamine neurons, which appears to be sensitive to D1 receptor activation, may be an effect that distinguishes typical and atypical antipyschotic agents.

摘要

从二羟基苯乙酸(DOPAC)浓度或多巴脱羧酶抑制后正中隆起中二羟基苯丙氨酸(DOPA)的积累判断,在急性给予所谓的非典型抗精神病药物氯氮平、硫利达嗪、美哌隆、塞托哌隆和RMI 81582后,结节漏斗多巴胺神经元的活性增加。相比之下,典型抗精神病药物氟哌啶醇、氯丙嗪、氟奋乃静、顺式氟哌噻吨或SCH 23390并未急性改变这些下丘脑多巴胺神经元的活性。非典型抗精神病药物对结节漏斗多巴胺神经元活性的急性刺激作用可被D1激动剂SKF 38393有效拮抗,但不能被D2激动剂喹吡罗拮抗。结节漏斗多巴胺神经元的急性激活似乎对D1受体激活敏感,这一效应可能是区分典型和非典型抗精神病药物的一个特征。

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