Medial prefrontal cortex (mPFC) and amygdala are closely interconnected brain areas that play a key role in cognitive-affective aspects of pain through their reciprocal interactions. Clinical and preclinical evidence suggests that dysfunctions in the mPFC-amygdala circuitry underlie pain-related cognitive-affective deficits. However, synaptic mechanisms of pain-related changes in these long-range pathways are largely unknown. Here we used optogenetics and brain slice physiology to analyze synaptic transmission in different types of amygdala neurons driven by inputs from infralimbic (IL) and prelimbic (PL) subdivisions of the mPFC. We found that IL inputs evoked stronger synaptic inhibition of neurons in the latero-capsular division of the central nucleus (CeLC) of the amygdala than PL inputs, and this inhibition was impaired in an arthritis pain model. Furthermore, inhibition-excitation ratio in basolateral amygdala neurons was increased in the pain model in the IL pathway but not in the PL pathway. These results suggest that IL rather than PL controls CeLC activity, and that changes in this acute pain model occur predominantly in the IL-amygdala pathway.

中文翻译：

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关节炎疼痛模型中皮质-杏仁核传递的途径特异性改变。

内侧前额叶皮层 (mPFC) 和杏仁核是紧密相连的大脑区域，它们通过相互作用在疼痛的认知情感方面发挥着关键作用。临床和临床前证据表明，mPFC-杏仁核回路的功能障碍是与疼痛相关的认知情感缺陷的基础。然而，这些长程通路中与疼痛相关的变化的突触机制在很大程度上是未知的。在这里，我们使用光遗传学和脑切片生理学来分析不同类型杏仁核神经元的突触传递，这些神经元由 mPFC 的边缘下 (IL) 和边缘前 (PL) 细分的输入驱动。我们发现，与 PL 输入相比，IL 输入对杏仁核中央核 (CeLC) 外侧囊分裂中的神经元产生更强的突触抑制，并且这种抑制在关节炎疼痛模型中受到损害。此外，在疼痛模型中，IL 通路中基底外侧杏仁核神经元的抑制-兴奋比增加，但 PL 通路中没有增加。这些结果表明 IL 而不是 PL 控制 CeLC 活性，并且这种急性疼痛模型的变化主要发生在 IL-杏仁核通路中。