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首页> 外文期刊>The European Journal of Neuroscience >CB1 augments mGluR5 function in medial prefrontal cortical neurons to inhibit amygdala hyperactivity in an arthritis pain model
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CB1 augments mGluR5 function in medial prefrontal cortical neurons to inhibit amygdala hyperactivity in an arthritis pain model

机译：CB1增强内侧前额叶皮层神经元中的mGluR5功能，以抑制关节炎疼痛模型中的杏仁核过度活跃

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The medial prefrontal cortex (mPFC) serves executive control functions and forms direct connections with subcortical areas such as the amygdala. Our previous work showed abnormal inhibition of mPFC pyramidal cells and hyperactivity of amygdala output neurons in an arthritis pain model. To restore mPFC activity and hence control pain-related amygdala hyperactivity this study focused on CB1 and mGluR5 receptors, which are important modulators of cortical functions. Extracellular single-unit recordings of infralimbic mPFC pyramidal cells and of amygdala output neurons in the laterocapsular division of the central nucleus (CeLC) were made in anesthetised adult male rats. mPFC neurons were classified as 'excited' or 'inhibited' based on their response to brief innocuous and noxious test stimuli. After arthritis pain induction, background activity and evoked responses of excited neurons and background activity and inhibition of inhibited neurons decreased. Stereotaxic application of an mGluR5-positive allosteric modulator (N-cyclobutyl-6-((3-fluorophenyl)ethynyl) nicotinamide hydrochloride, VU0360172) into the mPFC increased background and evoked activity of excited, but not inhibited, mPFC neurons under normal conditions but not in arthritis. A selective CB1 receptor agonist (arachidonyl-2-chloroethylamide) alone had no effect but restored the facilitatory effects of VU0360172 in the pain model. Coactivation of CB1 and mGluR5 in the mPFC inhibited the pain-related activity increase of CeLC neurons but had no effect under normal conditions. The data suggest that excited mPFC neurons are inversely linked to amygdala output (CeLC) and that CB1 can increase mGluR5 function in this subset of mPFC neurons to engage cortical control of abnormally enhanced amygdala output in pain.
机译：内侧前额叶皮层（mPFC）负责执行控制功能，并与皮质下区域（如杏仁核）形成直接连接。我们以前的工作显示出在关节炎疼痛模型中mPFC锥体细胞的异常抑制和杏仁核输出神经元的过度活跃。为了恢复mPFC活性，从而控制疼痛相关的杏仁核活动亢进，本研究集中于CB1和mGluR5受体，它们是皮质功能的重要调节剂。在麻醉的成年雄性大鼠中记录了下核mPFC锥体细胞和杏仁核输出核在中核后囊区（CeLC）的细胞外单单位记录。根据mPFC神经元对短暂的无害和有害测试刺激的反应，将其分为“兴奋”或“抑制”。关节炎疼痛诱导后，兴奋的神经元的背景活性和诱发的反应以及背景活性和抑制的神经元的抑制作用降低。在正常条件下将mGluR5阳性变构调节剂（N-环丁基-6-（（3-氟苯基）乙炔基）烟酰胺盐酸盐，VU0360172）立体定向施用会增加mPFC的本底和激发的但不受抑制的mPFC神经元的活性。不在关节炎中。单独的选择性CB1受体激动剂（花生四烯基-2-氯乙酰胺）无效，但在疼痛模型中恢复了VU0360172的促进作用。在mPFC中CB1和mGluR5的共激活抑制了CeLC神经元疼痛相关活性的增加，但在正常情况下没有作用。数据表明，兴奋的mPFC神经元与杏仁核输出（CeLC）反向关联，并且CB1可以增加该mPFC神经元子集中的mGluR5功能，从而参与疼痛中异常增强的杏仁核输出的皮质控制。

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