Rezayof Ameneh, Hosseini Sedighe-Sadat, Zarrindast Mohammad-Reza
Department of Animal Biology, School of Biology, College of Science, University of Tehran, Tehran, Iran.
Behav Brain Res. 2009 Sep 14;202(2):171-8. doi: 10.1016/j.bbr.2009.03.030. Epub 2009 Apr 1.
The objective of the present study was to evaluate the possible role of dopamine D(1)/D(2) receptors of the central amygdala (CeA) on morphine-induced anxiolytic-like behaviour in adult male Wistar rats. The animals were bilaterally implanted with chronic cannulas the CeA and tested in an elevated plus maze (EPM) task. Intraperitoneal (i.p.) administration of morphine (5 and 6 mg/kg) increased the percentage of open arm time (%OAT) and open arm entries (%OAE), indicating an anxiolytic-like response. Intra-CeA administration of different doses of the dopaminergic agonist apomorphine (0.1-0.3 microg/rat) significantly increased %OAE, but not %OAT. Furthermore, co-administration of the same doses of apomorphine with an ineffective dose of morphine (4 mg/kg; i.p.) significantly increased %OAT and %OAE by the opioid. Single microinjection of the D(1) dopaminergic antagonist SCH23390 (0.5-1.5 microg/rat) or sulpiride (0.5-1.5 microg/rat) into the CeA caused no significant change for %OAT and %OAE. The obtained results also show that intra-CeA microinjection of the same doses of SCH23390 or sulpiride inhibits the anxiolytic-like effect of morphine (6 mg/kg; i.p.). Pre-treatment of animals with SCH23390 (intra-CeA) or sulpiride (intra-CeA) reversed the response induced by apomorphine (0.3 microg/rat) plus morphine (4 mg/kg; i.p.). It should be considered that the drugs also did not show any effect on locomotor activity in all experiments. In conclusion, these findings suggest that the central amygdala dopaminergic mechanisms, probably via D(1)/D(2) receptors, may be involved in the modulation of morphine-induced anxiolytic-like behaviour in rat.
本研究的目的是评估成年雄性Wistar大鼠中央杏仁核(CeA)的多巴胺D(1)/D(2)受体在吗啡诱导的抗焦虑样行为中可能发挥的作用。给动物双侧植入慢性套管于CeA,并在高架十字迷宫(EPM)任务中进行测试。腹腔注射(i.p.)吗啡(5和6 mg/kg)增加了开放臂时间百分比(%OAT)和开放臂进入次数百分比(%OAE),表明出现了抗焦虑样反应。向CeA内注射不同剂量的多巴胺能激动剂阿扑吗啡(0.1 - 0.3 μg/大鼠)显著增加了%OAE,但未增加%OAT。此外,将相同剂量的阿扑吗啡与无效剂量的吗啡(4 mg/kg;i.p.)联合给药,可显著增加阿片类药物引起的%OAT和%OAE。向CeA内单次微量注射D(1)多巴胺能拮抗剂SCH23390(0.5 - 1.5 μg/大鼠)或舒必利(0.5 - 1.5 μg/大鼠),对%OAT和%OAE没有显著影响。所得结果还表明,向CeA内微量注射相同剂量的SCH23390或舒必利可抑制吗啡(6 mg/kg;i.p.)的抗焦虑样作用。用SCH23390(CeA内)或舒必利(CeA内)对动物进行预处理,可逆转阿扑吗啡(0.3 μg/大鼠)加吗啡(4 mg/kg;i.p.)诱导的反应。应该注意的是,在所有实验中这些药物对运动活动也没有任何影响。总之,这些发现表明,中央杏仁核多巴胺能机制可能通过D(1)/D(2)受体参与调节大鼠吗啡诱导的抗焦虑样行为。