Department of Anatomy and K.K. Leung Brain Research Centre, Fourth Military Medical University, Xi'an 710032, China.
Institute of Medical Research, Northwestern Polytechnical University, Xi'an 710072, China.
Neuron. 2022 Jun 15;110(12):1993-2008.e6. doi: 10.1016/j.neuron.2022.03.030. Epub 2022 Apr 19.
Empathic pain has attracted the interest of a substantial number of researchers studying the social transfer of pain in the sociological, psychological, and neuroscience fields. However, the neural mechanism of empathic pain remains elusive. Here, we establish a long-term observational pain model in mice and find that glutamatergic projection from the insular cortex (IC) to the basolateral amygdala (BLA) is critical for the formation of observational pain. The selective activation or inhibition of the IC-BLA projection pathway strengthens or weakens the intensity of observational pain, respectively. The synaptic molecules are screened, and the upregulated synaptotagmin-2 and RIM3 are identified as key signals in controlling the increased synaptic glutamate transmission from the IC to the BLA. Together, these results reveal the molecular and synaptic mechanisms of a previously unidentified neural pathway that regulates observational pain in mice.
共情痛引起了大量研究人员的兴趣，这些研究人员分别来自社会学、心理学和神经科学领域，他们研究社会传递的痛觉。然而，共情痛的神经机制仍难以捉摸。在这里，我们在小鼠中建立了一个长期观察性疼痛模型，发现从脑岛（IC）到基底外侧杏仁核（BLA）的谷氨酸能投射对于观察性疼痛的形成至关重要。选择性激活或抑制 IC-BLA 投射途径分别增强或减弱观察性疼痛的强度。筛选突触分子，上调的突触结合蛋白-2 和 RIM3 被鉴定为控制从 IC 到 BLA 的突触谷氨酸传递增加的关键信号。总之，这些结果揭示了一个以前未被识别的神经通路的分子和突触机制，该通路调节小鼠的观察性疼痛。
