Abstract
Pain is an unpleasant experience with both sensory and affective components. However, the neural circuits underlying modulation of pain-related behaviors remains unclear. In this study, we identified an inhibitory neural circuit that originates in central amygdala protein kinase C-delta (CeA-PKCδ) neurons and terminates in the ventral sector of the zona incerta (ZI), a subthalamic structure previously linked to pain processing. Behavioral experiments show that chemogenetic inhibition of GABAergic ZI neurons induces bilateral hypersensitivity in uninjured mice as well as contralateral hypersensitivity after nerve injury. In contrast, chemogenetic activation of VGAT cells in the ZI reverses nerve injury-induced hypersensitivity. Furthermore, we found that chemogenetic activation of ZI-VGAT neurons reduced pain-related aversion during formalin conditioned place aversion (FCPA) without affecting spontaneous nociceptive responses induced by formalin. Taken together, our results suggest an indispensable role of ZI in regulating somatosensory and affective components of pain. Grant support from NCCIH.
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