Events

Dr. Bo Duan received a bachelor’s degree in polymer chemistry at the University of Sciences and Technology of China in 2002. He earned his PhD degree in Neuroscience at the Institute of Neuroscience, Chinese Academy of Sciences in 2007 and kept working there until 2010. He did his postdoctoral work at Harvard Medical School from 2010-2016. Dr. Duan joined the faculty at the University of Michigan as an Assistant Professor in 2016 and was promoted to tenured associate professor in 2023. His primary appointment is in the Department of Molecular, Cellular, and Developmental Biology, and he is affiliated with the Neuroscience Graduate Program, the Michigan Neuroscience Institute, the Kresge Hearing Research Institute, the Skin Biology and Diseases Resource-Based Center, and the Center for Cell Plasticity and Organ Design.

External temperature perception is crucial for maintaining homeostasis and preventing temperature-related injuries. While progress has been made in identifying molecular thermosensors, the neural circuits involved in temperature signaling remain largely unknown. Here we unveil the spinal circuit transmitting skin-to-brain cool signals. Excitatory interneurons in the dorsal horn, co-expressing Calbindin1 and Thyrotropin-releasing hormone receptor (Calb1_Trhr), act as a central hub for cool sensation. Calb1_Trhr neurons receive inputs from Transient receptor potential melastatin type 8-positive (TRPM8+) sensory afferents in the dorsal root ganglion. Genetic ablation or silencing of Calb1_Trhr neurons results in the loss of cool sensation. Calcitonin receptor-like receptor (Calcrl+) expressing spinal projection neurons receive inputs from both Calb1Trhr neurons and TRPM8+ afferents and transmit cool signals to the parabrachial nucleus in the brain. Calb1_Trhr neuron absence impedes activation of Calcrl+ neurons, preventing cool transmission. Our study has provided a comprehensive depiction of the neural architecture for temperature sensation.