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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Potentiation of dopamine D1-like receptor signaling by concomitant activation of δ- And μ-opioid receptors in mouse medial prefrontal cortex
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Potentiation of dopamine D1-like receptor signaling by concomitant activation of δ- And μ-opioid receptors in mouse medial prefrontal cortex

机译：通过同时激活小鼠内侧前额叶皮层中的δ和μ阿片受体激活多巴胺D1样受体信号

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Opioid receptors located in the ventral tegmental area are known to regulate dopamine (DA) release from mesocortical afferents to medial prefrontal cortex (mPFC) but little is known on whether in this cortical region activation of opioid receptors affect DA receptor signaling. In the present study we show that in mouse mPFC concomitant activation of either δ- or μ-opioid receptors, but not κ-opioid receptors, potentiated DA D1-like receptor-induced stimulation of adenylyl cyclase activity through a G protein βγ subunit-dependent mechanism. In tissue slices of mPFC, the combined addition of the opioid agonist leu-enkephalin and the DA D1-like receptor agonist SKF 81297 produced more than additive increase in the phosphorylation state of AMPA and NMDA receptor subunits GluR1 and NR1, respectively. Moreover, in primary cultures of mouse frontal cortex neurons, DA D1-like receptor-induced Ser133 phosphorylation of the transcription factor cyclic AMP responsive element binding protein was potentiated by concurrent stimulation of opioid receptors. Double immunofluorescence analysis of cultured cortical cells indicated that a large percentage of DA D1 receptor positive cells expressed either δ- or μ-opioid receptor immunoreactivity. These data indicate that in mouse mPFC activation of μ- and δ-opioid receptors enhances DA D1-like receptor signaling likely through converging regulatory inputs on βγ-stimulated adenylyl cyclase isoforms. This previously unrecognized synergistic interaction may selectively affect DA D1 transmission at specific postsynaptic sites where the receptors are co-localized and may play a role in prefrontal DA D1 regulation of opioid addiction.
机译：已知位于腹侧被盖区的阿片受体调节多巴胺（DA）从中皮层传入到内侧前额叶皮层（mPFC）的释放，但对于在此皮层区域中阿片受体的激活是否影响DA受体的信号知之甚少。在本研究中，我们表明，在小鼠mPFC中，δ或μ阿片受体但不激活κ阿片受体同时激活，增强了D D1样受体诱导的G蛋白βγ亚基依赖性对腺苷酸环化酶活性的刺激。机制。在mPFC的组织切片中，阿片类激动剂亮脑啡肽和DA D1样受体激动剂SKF 81297的联合添加分别使AMPA和NMDA受体亚基GluR1和NR1的磷酸化状态增加了更多。此外，在小鼠额叶皮层神经元的原代培养中，DA D1样受体诱导的转录因子环AMP响应元件结合蛋白的Ser133磷酸化通过同时刺激阿片受体来增强。对培养的皮层细胞进行的双重免疫荧光分析表明，大部分DA D1受体阳性细胞表达δ-或μ-阿片受体的免疫反应性。这些数据表明，在小鼠mPFC中，μ和δ阿片受体的激活可能会增强DA D1样受体的信号传导，这可能是通过将受βγ刺激的腺苷酸环化酶同工型的调节输入汇合而实现的。这种先前无法识别的协同相互作用可能选择性地影响DA D1在特定的突触后位点的传递，在这些位点受体是共定位的，并且可能在前额叶DA D1对阿片类药物成瘾的调节中发挥作用。

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