A craniofacial-specific monosynaptic circuit enables heightened affective pain.
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Humans often rank craniofacial pain as more severe than body pain. Evidence suggests that a stimulus of the same intensity induces stronger pain in the face than in the body. However, the underlying neural circuitry for the differential processing of facial versus bodily pain remains unknown. Interestingly, the lateral parabrachial nucleus (PBL), a critical node in the affective pain circuit, is activated more strongly by noxious stimulation of the face than of the hindpaw. Using a novel activity-dependent technology called CANE developed in our laboratory, we identified and selectively labeled noxious-stimulus-activated PBL neurons and performed comprehensive anatomical input-output mapping. Surprisingly, we uncovered a hitherto uncharacterized monosynaptic connection between cranial sensory neurons and the PBL-nociceptive neurons. Optogenetic activation of this monosynaptic craniofacial-to-PBL projection induced robust escape and avoidance behaviors and stress calls, whereas optogenetic silencing specifically reduced facial nociception. The monosynaptic circuit revealed here provides a neural substrate for heightened craniofacial affective pain.
Mice, Inbred C57BL
Published Version (Please cite this version)10.1038/s41593-017-0012-1
Publication InfoYin, Henry; Wang, Fan; Chen, Yong; Rodriguez, Erica; Sakurai, Katsuyasu; Xu, Jennie; ... Liedtke, Wolfgang (2017). A craniofacial-specific monosynaptic circuit enables heightened affective pain. Nature neuroscience, 20(12). pp. 1734-1743. 10.1038/s41593-017-0012-1. Retrieved from https://hdl.handle.net/10161/17673.
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Assistant Professor in Neurology
Morris N. Broad Distinguished Professor
My lab studies neural circuit basis of sensory perception. Specifically we are interested in determining neural circuits underlying (1) active touch sensation including tactile processing stream and motor control of touch sensors on the face; (2) pain sensation including both sensory-discriminative and affective aspects of pain; and (3) general anesthesia including the active pain-suppression process. We use a combination of genetic, viral, electrophysiology, and in vivo imaging (in f
Associate Professor in the Department of Psychology and Neuroscience
I am interested in understanding the neural mechanisms underlying goal-directed actions. For the first time in history, advances in psychology and neurobiology have made it feasible to pursue the detailed neural mechanisms underlying goal-directed and voluntary actions--how they are driven by the needs and desires of the organism and controlled by cognitive processes that provide a rich representation of the self and the world. My approach to this problem is highly integrative, combining behav
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