• Shuohao Sun, Qian Xu, Changxiong Guo, Yun Guan, Qin Liu, and Xinzhong Dong.
• The Solomon H. Snyder Department of Neuroscience and Center for Sensory Biology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
• Neuron. 2017 Feb 22; 93 (4): 840-853.e5.

AbstractCoding of itch versus pain has been heatedly debated for decades. However, the current coding theories (labeled line, intensity, and selectivity theory) cannot accommodate all experimental observations. Here we identified a subset of spinal interneurons, labeled by gastrin-releasing peptide (Grp), that receive direct synaptic input from both pain and itch primary sensory neurons. When activated, these Grp+ neurons generated rarely seen, simultaneous robust pain and itch responses that were intensity dependent. Accordingly, we propose a "leaky gate" model in which Grp+ neurons transmit both itch and weak pain signals; however, upon strong painful stimuli, the recruitment of endogenous opioids works to close this gate, reducing overwhelming pain generated by parallel pathways. Consistent with our model, loss of these Grp+ neurons increased pain responses while itch was decreased. Our new model serves as an example of non-monotonic coding in the spinal cord and better explains observations in human psychophysical studies.Copyright © 2017 Elsevier Inc. All rights reserved.

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