Somatosensory autonomic reflexes allow electroacupuncture stimulation (ES) to modulate body physiology at distant sites^1,2,3,4,5,6 (for example, suppressing severe systemic inflammation^6,7,8,9). Since the 1970s, an emerging organizational rule about these reflexes has been the presence of body-region specificity^1,2,3,4,5,6. For example, ES at the hindlimb ST36 acupoint but not the abdominal ST25 acupoint can drive the vagal–adrenal anti-inflammatory axis in mice^10,11. The neuroanatomical basis of this somatotopic organization is, however, unknown. Here we show that PROKR2^Cre-marked sensory neurons, which innervate the deep hindlimb fascia (for example, the periosteum) but not abdominal fascia (for example, the peritoneum), are crucial for driving the vagal–adrenal axis. Low-intensity ES at the ST36 site in mice with ablated PROKR2^Cre-marked sensory neurons failed to activate hindbrain vagal efferent neurons or to drive catecholamine release from adrenal glands. As a result, ES no longer suppressed systemic inflammation induced by bacterial endotoxins. By contrast, spinal sympathetic reflexes evoked by high-intensity ES at both ST25 and ST36 sites were unaffected. We also show that optogenetic stimulation of PROKR2^Cre-marked nerve terminals through the ST36 site is sufficient to drive the vagal–adrenal axis but not sympathetic reflexes. Furthermore, the distribution patterns of PROKR2^Cre nerve fibres can retrospectively predict body regions at which low-intensity ES will or will not effectively produce anti-inflammatory effects. Our studies provide a neuroanatomical basis for the selectivity and specificity of acupoints in driving specific autonomic pathways.

体感自主神经反射允许电针刺激 (ES) 调节远处部位的身体生理机能^1,2,3,4,5,6（例如，抑制严重的全身性炎症^6,7,8,9）。^{自 1970 年代以来，关于这些反射的新兴组织规则一直是身体区域特异性1,2,3,4,5,6}的存在。例如，后肢 ST36 穴位而非腹部 ST25 穴位的 ES 可以驱动小鼠的迷走神经-肾上腺抗炎轴^10,11。然而，这种躯体组织的神经解剖学基础尚不清楚。在这里我们展示了 PROKR2 ^Cre标记的感觉神经元支配后肢深筋膜（例如，骨膜）而不是腹部筋膜（例如，腹膜），对于驱动迷走神经 - 肾上腺轴至关重要。在具有消融的 PROKR2 ^Cre标记的感觉神经元的小鼠中，ST36 位点的低强度 ES 无法激活后脑迷走神经传出神经元或驱动儿茶酚胺从肾上腺释放。结果，ES 不再抑制由细菌内毒素引起的全身性炎症。相比之下，高强度 ES 在 ST25 和 ST36 位点诱发的脊髓交感神经反射未受影响。我们还表明 PROKR2 ^{Cre的光遗传学刺激}通过 ST36 部位的标记神经末梢足以驱动迷走神经-肾上腺轴，但不能驱动交感神经反射。^{此外，PROKR2 Cre}神经纤维的分布模式可以回顾性预测低强度 ES 会或不会有效产生抗炎作用的身体区域。我们的研究为穴位在驱动特定自主神经通路中的选择性和特异性提供了神经解剖学基础。