Neural mechanisms of reflex facilitation and inhibition of gastric motility to stimulation of various skin areas in rats. Our studies provide a neuroanatomical basis for the selectivity and specificity of acupoints in driving specific autonomic pathways. 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. 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. By contrast, spinal sympathetic reflexes evoked by high-intensity ES at both ST25 and ST36 sites were unaffected. As a result, ES no longer suppressed systemic inflammation induced by bacterial endotoxins. 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. 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.
The neuroanatomical basis of this somatotopic organization is, however, unknown.
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. Since the 1970s, an emerging organizational rule about these reflexes has been the presence of body-region specificity 1, 2, 3, 4, 5, 6. 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).