| First Author | Segelcke D | Year | 2021 |
| Journal | Cell Rep | Volume | 37 |
| Issue | 12 | Pages | 110152 |
| PubMed ID | 34936870 | Mgi Jnum | J:328221 |
| Mgi Id | MGI:6881786 | Doi | 10.1016/j.celrep.2021.110152 |
| Citation | Segelcke D, et al. (2021) Tmem160 contributes to the establishment of discrete nerve injury-induced pain behaviors in male mice. Cell Rep 37(12):110152 |
| abstractText | 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. |
