Author: Shenbin Liu#1,2,3,4, Zhifu Wang#1, Yangshuai Su1,5, Lu Qi1, Wei Yang1, Mingzhou Fu1, Xianghong Jing5, Yanqing Wang2,3,4, Qiufu Ma6
1 Dana-Farber Cancer Institute and Department of Neurobiology, Harvard Medical School, Boston, MA, USA.
2 Institute of Acupuncture and Moxibustion, Fudan Institutes of Integrative Medicine, Fudan University, Shanghai, China.
3 Department of Integrative Medicine and Neurobiology, School of Basic Medical Science, Fudan University, Shanghai, China.
4 State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, Fudan University, Shanghai, China.
5 Meridians Research Center, Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, Beijing, China.
6 Dana-Farber Cancer Institute and Department of Neurobiology, Harvard Medical School, Boston, MA, USA. Qiufu_Ma@dfci.harvard.edu.
Date published: 2021 Oct 1
Other: Volume ID: 598 , Issue ID: 7882 , Pages: 641-645 , Special Notes: doi: 10.1038/s41586-021-04001-4. , Word Count: 240
Somatosensory autonomic reflexes allow electroacupuncture stimulation (ES) to modulate body physiology at distant sites1-6 (for example, suppressing severe systemic inflammation6-9). Since the 1970s, an emerging organizational rule about these reflexes has been the presence of body-region specificity1-6. For example, ES at the hindlimb ST36 acupoint but not the abdominal ST25 acupoint can drive the vagal-adrenal anti-inflammatory axis in mice10,11. The neuroanatomical basis of this somatotopic organization is, however, unknown. Here we show that PROKR2Cre-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 PROKR2Cre-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 PROKR2Cre-marked nerve terminals through the ST36 site is sufficient to drive the vagal-adrenal axis but not sympathetic reflexes. Furthermore, the distribution patterns of PROKR2Cre 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.
PMID: 34646018 DOI: 10.1038/s41586-021-04001-4