Milnacipran enhances the control of impulsive action by activating D_1-like receptors in the infralimbic cortex.

Milnacipran enhances the control of impulsive action by activating D_1-like receptors in the infralimbic cortex.
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米那普仑通过激活边缘下皮质中的 D_1 样受体来增强对冲动行为的控制。

DOI:
10.1007/s00213-012-2835-5
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发表时间:
2013
期刊:
Psychopharmacology (Berl)
影响因子:
--
通讯作者:
Yamaguchi
Yamaguchi
中科院分区:
--
文献类型:
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作者:
Tsutsui-Kimura I;Ohmura Y;Izumi T;Kumamoto H;Yamaguchi

文献摘要

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抑郁症患者经常会出现冲动性升高。我们最近发现,米那普仑,一种抗抑郁药和血清素/去甲肾上腺素再摄取抑制剂,可以增强大鼠的冲动控制。然而,米那普仑对冲动行为影响的神经机制仍不清楚。米那普仑不仅增加细胞外5-羟色胺和去甲肾上腺素,而且还增加多巴胺特别是在内侧前额叶皮层,这是一个大脑区域负责冲动action.ObjectivesOur的目标是要确定是否D1-和/或D2-样受体在下边缘皮层(IL),腹侧部分的内侧前额叶皮层,在三选择系列反应时间任务中介导米那西泮增强的冲动控制。方法大鼠双侧注射选择性D1样受体拮抗剂SCH 23390(0.3或3 ng/侧)或依替氯必利(一种选择性D2样受体拮抗剂)米那普仑急性腹腔内给药后(0.3或1 μg/侧)进入IL结果IL SCH 23390内注射逆转了米那普仑增强的冲动控制,而依替氯必利注射到IL中未能阻断米那普仑对冲动action.ConclusionsThis的影响,这是第一份报告,证明了一个关键的作用,为D1样受体的IL在米那普仑增强控制冲动的行动。
RationaleElevated impulsivity is often observed in patients with depression. We recently found that milnacipran, an antidepressant and a serotonin/noradrenaline reuptake inhibitor, could enhance impulse control in rats. However, the neural mechanisms underlying the effects of milnacipran on impulsive action remain unclear. Milnacipran increases not only extracellular serotonin and noradrenaline but also dopamine specifically in the medial prefrontal cortex, which is one of the brain regions responsible for impulsive action.ObjectivesOur goal was to identify whether D1- and/or D2-like receptors in the infralimbic cortex (IL), the ventral portion of the medial prefrontal cortex, mediates the milnacipran-enhanced impulse control in a three-choice serial reaction time task.MethodsThe rats were bilaterally injected with SCH23390, a selective D1-like receptor antagonist (0.3 or 3 ng/side) or eticlopride, a selective D2-like receptor antagonist (0.3 or 1 μg/side) into the IL after acute intraperitoneal administration of milnacipran (10 mg/kg).ResultsIntra-IL SCH23390 injections reversed the milnacipran-enhanced impulse control, whereas injections of eticlopride into the IL failed to block the effects of milnacipran on impulsive action.ConclusionsThis is the first report that demonstrates a critical role for D1-like receptors of the IL in milnacipran-enhanced control of impulsive action.