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首页> 外文期刊>European neuropsychopharmacology: the journal of the European College of Neuropsychopharmacology >Neuropeptide Y in the central nucleus of amygdala regulates the anxiolytic effect of agmatine in rats
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Neuropeptide Y in the central nucleus of amygdala regulates the anxiolytic effect of agmatine in rats

机译:杏仁核中央核中的神经肽Y调节胍丁胺在大鼠中的抗焦虑作用

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In the present study, modulation of anxiolytic action of agmatine by neuropeptide Y (NPY) in the central nucleus of amygdala (CeA) is evaluated employing Vogel's conflict test (VCT) in rats. The intra-CeA administration of agmatine (0.6 and 1.2μmol/rat), NPY (10 and 20pmol/rat) or NPY Y1/Y5 receptors agonist [Leu31, Pro34]-NPY (30 and 60pmol/rat) significantly increased the number of punished drinking licks following 15min of treatment. Combination treatment of subeffective dose of NPY (5pmol/rat) or [Leu31, Pro34]-NPY (15pmol/rat) and agmatine (0.3μmol/rat) produced synergistic anxiolytic-like effect. However, intra-CeA administration of selective NPY Y1 receptor antagonist, BIBP3226 (0.25 and 0.5mmol/rat) produced anxiogenic effect. In separate set of experiment, pretreatment with BIBP3226 (0.12mmol/rat) reversed the anxiolytic effect of agmatine (0.6μmol/rat). Furthermore, we evaluated the effect of intraperitoneal injection of agmatine (40mg/kg) on NPY-immunoreactivity in the nucleus accumbens shell (AcbSh), lateral part of bed nucleus of stria terminalis (BNSTl) and CeA. While agmatine treatment significantly decreased the fibers density in BNSTl, increase was noticed in AcbSh. In addition, agmatine reduced NPY-immunoreactive cells in the AcbSh and CeA. Immunohistochemical data suggest the enhanced transmission of NPY from the AcbSh and CeA. Taken together, this study suggests that agmatine produced anxiolytic effect which might be regulated via modulation of NPYergic system particularly in the CeA.
机译:在本研究中,使用Vogel冲突试验(VCT)对大鼠杏仁核中央核(CeA)中的神经肽Y(NPY)调节胍丁胺的抗焦虑作用进行了评估。胍丁胺(0.6和1.2μmol/大鼠),NPY(10和20 pmol/大鼠)或NPY Y1 / Y5受体激动剂[Leu31,Pro34] -NPY(30和60 pmol/大鼠)的CeA内给药显着增加了治疗15分钟后,应惩罚饮酒舔。亚有效剂量的NPY(5 pmol/大鼠)或[Leu31,Pro34] -NPY(15 pmol/大鼠)和胍丁胺(0.3μmol/大鼠)的联合治疗产生协同抗焦虑作用。然而,CeA内的选择性NPY Y1受体拮抗剂BIBP3226(0.25和0.5mmol /大鼠)的产生焦虑作用。在另一组实验中,用BIBP3226(0.12mmol / rat)进行的预处理逆转了胍丁胺(0.6μmol/ rat)的抗焦虑作用。此外,我们评估了腹腔内注射胍丁胺(40mg / kg)对伏伏核壳(AcbSh),末梢纹床核外侧(BNST1)和CeA中NPY-免疫反应性的影响。尽管胍丁胺处理显着降低了BNST1中的纤维密度,但在AcbSh中却注意到了增加。此外,胍丁胺可减少AcbSh和CeA中的NPY免疫反应性细胞。免疫组化数据表明,AcbSh和CeA增强了NPY的传播。两者合计,这项研究表明,胍丁胺产生抗焦虑作用,这可以通过调节NPYergic系统来调节,特别是在CeA中。

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