Titel
Tmem160 contributes to the establishment of discrete nerve injury-induced pain behaviors in male mice
Autor*in
Daniel Segelcke
Department of Anaesthesiology, Intensive Care and Pain Medicine, University Hospital Muenster
Meike Hütte
Somatosensory Signaling and Systems Biology, Max Planck Institute of Experimental Medicine
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Abstract
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.
Stichwort
chronic painneuropathic painmouse pain behaviorcytokinespain initiationneuro-immune interactionnerve injurydorsal root gangliainflammatory signaling
Objekt-Typ
Sprache
Englisch [eng]
Persistent identifier
Erschienen in
Titel
Cell Reports
Band
37
Ausgabe
12
ISSN
2211-1247
Erscheinungsdatum
2021
Publication
Elsevier BV
Erscheinungsdatum
2021
Zugänglichkeit
Rechte
Rechteangabe
(c) 2021 The Author(s)
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