Tmem160 contributes to the establishment of discrete nerve injury-induced pain behaviors in male mice
- Cell Rep. 2021 Dec 21;37(12):110152. doi: 10.1016/j.celrep.2021.110152.
- 1. Department of Anaesthesiology, Intensive Care and Pain Medicine, University Hospital Muenster, Muenster, Germany.
- 2. Division of Pharmacology and Toxicology, Department of Pharmaceutical Sciences, University of Vienna, Vienna, Austria.
- 3. Somatosensory Signaling and Systems Biology, Max Planck Institute of Experimental Medicine, Goettingen, Germany.
- 4. Department of Cellular Biochemistry, University Medical Center Goettingen, Goettingen, Germany.
- 5. Department of Molecular Neurobiology, Max Planck Institute of Experimental Medicine, Goettingen, Germany.
- 6. Division of Pharmacology and Toxicology, Department of Pharmaceutical Sciences, University of Vienna, Vienna, Austria. Electronic address: [email protected].
Chronic Pain is a prevalent medical problem, and its molecular basis remains poorly understood. Here, we demonstrate the significance of the transmembrane protein (Tmem) 160 for nerve injury-induced neuropathic Pain. An extensive behavioral assessment suggests a Pain modality- and entity-specific phenotype in male Tmem160 global knockout (KO) mice: delayed establishment of tactile hypersensitivity and alterations in self-grooming after nerve injury. In contrast, Tmem160 seems to be dispensable for other nerve injury-induced Pain modalities, such as non-evoked and movement-evoked Pain, and for other Pain entities. Mechanistically, we show that global KO males exhibit dampened neuroimmune signaling and diminished TRPA1-mediated activity in cultured dorsal root ganglia. Neither these changes nor altered pain-related behaviors are observed in global KO female and male peripheral sensory neuron-specific KO mice. Our findings reveal Tmem160 as a sexually dimorphic factor contributing to the establishment, but not maintenance, of discrete nerve injury-induced Pain behaviors in male mice.