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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