目的 探讨小鼠内侧前额叶皮质（mPFC）-丘脑室旁核（PVT）通路的投射神经元性质及调控该通路对生理痛和急性痛的影响。方法  将CTb注入GAD67-GFP转基因小鼠的PVT内，观察向PVT投射的mPFC神经元的性质，使用化学遗传学方法调控mPFC-PVT通路，观察对小鼠机械痛、热痛和冷痛以及辣椒素诱导的急性炎性痛的影响。结果 mPFC内CTb标记神经元主要分布于V层和VI层且与GAD67-GFP不共标；化学遗传学方法激活mPFC-PVT通路可显著降低小鼠的机械痛阈值（p < 0.0001），缩小热痛潜伏期（p < 0.001），对冷痛无明显的影响，抑制此通路则可显著提高动物的机械性痛阈（p < 0.05）；辣椒素诱导急性炎性痛模型下激活此通路引起小鼠舔爪时间增加（p < 0.05）。结论 mPFC-PVT通路为非GABA能的神经通路，激活该通路可促进小鼠的机械痛、热痛、急性炎性痛反应。

Objective  To explore the neuronal properties of the pathway from the medial prefrontal cortex (mPFC) to the paraventricular thalamic nucleus of (PVT) and to investigate the effect of modulation of the pathway on physiological pain and acute pain in mice. Methods  CTb was injected into the PVT of GAD67-GFP transgenic mice, and the properties of mPFC neurons projected to PVT were observed. The mPFC-PVT pathway was activated or inhibited by chemogenetics to observe the effects on physiological pain, such as mechanical pain, thermal pain, cold pain, and on capsaicin induced inflammatory pain. Results  CTB-labeled neurons in the mPFC were mainly distributed in layer V and layer VI, and were not double-labeled with GAD67-GFP. Chemogenetic activation of the mPFC-PVT pathway significantly decreased the mechanical pain threshold (p < 0.0001) and shortened the thermal pain latency (p < 0.001), but had no obvious effects on cold pain. Inhibition of this pathway significantly increased the mechanical pain threshold (p < 0.05). Activation of the pathway increased the paw licking time (p < 0.05) in acute inflammatory pain induced by intraplantar injection of capsaicin. Conclusion  mPFC-PVT pathway is a non GABAergic projection and its activation can promote mechanical pain, thermal pain, and acute inflammatory pain in mice.