Fig. 10. Schematic summary of the main findings illustrating how activity in the LPBN circuit governs physiological and pathological pain-like hypersensitivity.

a Light-activation of glutamatergic neurons induces hyperalgesia in naive mice to an extent similar to that in CPN-ligated mice. b Light-inactivation of glutamatergic neurons induces analgesia in both naive and CPN-ligated mice. c Daily pharmacogenetic activation of glutamatergic neurons for one week induces chronic nociception, mimicking neuropathic pain. d Light-activation of GABAergic neurons inhibits neuropathic pain-like hypersensitivity, but not basal nociception. e Light-inactivation of GABAergic neurons induces hyperalgesia in naive mice to an extent similar to that in CPN-ligated mice. f Daily pharmacogenetic activation of GABAergic neurons for one week prevents the development of neuropathic pain-like hypersensitivity in CPN-ligated mice.