Kuroki Toshihide, Meltzer Herbert Y, Ichikawa Junji
Department of Neuropsychiatry, Kyushu University Graduate School of Medical Science, Maidashi 3-1-1, Higashiku, Fukuoka 812-8582, Japan.
Brain Res. 2003 May 16;972(1-2):216-21. doi: 10.1016/s0006-8993(03)02516-2.
(+/-)-([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.
(±)-([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。