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DOI(一种5-HT 2A/2C受体激动剂)对5-HT 2A受体的刺激增强了苯丙胺诱导的大鼠内侧前额叶皮质和伏隔核中的多巴胺释放。

5-HT 2A receptor stimulation by DOI, a 5-HT 2A/2C receptor agonist, potentiates amphetamine-induced dopamine release in rat medial prefrontal cortex and nucleus accumbens.

作者信息

Kuroki Toshihide, Meltzer Herbert Y, Ichikawa Junji

机构信息

Department of Neuropsychiatry, Kyushu University Graduate School of Medical Science, Maidashi 3-1-1, Higashiku, Fukuoka 812-8582, Japan.

出版信息

Brain Res. 2003 May 16;972(1-2):216-21. doi: 10.1016/s0006-8993(03)02516-2.

Abstract

(+/-)-([1-(2,5-Dimethoxy-4-iodophenyl)-aminopropane]-hydrochloride) (DOI) (2.5 mg/kg), a 5-HT(2A/2C) agonist, significantly potentiated D-amphetamine (AMPH) (1 mg/kg)-induced dopamine (DA) release in rat medial prefrontal cortex (mPFC) and nucleus accumbens (NAC). This effect of DOI was completely prevented by M100907 (1 mg/kg), a selective 5-HT(2A) antagonist, which by itself had no effect on basal and AMPH-induced DA release in either region. Thus, 5-HT(2A) receptor agonism potentiates AMPH-induced DA release in the mPFC and NAC.

摘要

(±)-([1-(2,5-二甲氧基-4-碘苯基)-氨基丙烷]-盐酸盐)(DOI)(2.5毫克/千克),一种5-羟色胺(5-HT)(2A/2C)激动剂,显著增强了D-苯丙胺(AMPH)(1毫克/千克)诱导的大鼠内侧前额叶皮质(mPFC)和伏隔核(NAC)中的多巴胺(DA)释放。DOI的这种作用被选择性5-HT(2A)拮抗剂M100907(1毫克/千克)完全阻断,而M100907本身对这两个区域的基础和AMPH诱导的DA释放均无影响。因此,5-HT(2A)受体激动作用增强了mPFC和NAC中AMPH诱导的DA释放。

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