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Chemokine Receptor CXCR3 in the Spinal Cord Contributes to Chronic Itch in Mice / 神经科学通报·英文版
Neuroscience Bulletin ; (6): 54-63, 2018.
Article en En | WPRIM | ID: wpr-777080
Biblioteca responsable: WPRO
ABSTRACT
Recent studies have shown that the chemokine receptor CXCR3 and its ligand CXCL10 in the dorsal root ganglion mediate itch in experimental allergic contact dermatitis (ACD). CXCR3 in the spinal cord also contributes to the maintenance of neuropathic pain. However, whether spinal CXCR3 is involved in acute or chronic itch remains unclear. Here, we report that Cxcr3 mice showed normal scratching in acute itch models but reduced scratching in chronic itch models of dry skin and ACD. In contrast, both formalin-induced acute pain and complete Freund's adjuvant-induced chronic inflammatory pain were reduced in Cxcr3 mice. In addition, the expression of CXCR3 and CXCL10 was increased in the spinal cord in the dry skin model induced by acetone and diethyl ether followed by water (AEW). Intrathecal injection of a CXCR3 antagonist alleviated AEW-induced itch. Furthermore, touch-elicited itch (alloknesis) after compound 48/80 or AEW treatment was suppressed in Cxcr3 mice. Finally, AEW-induced astrocyte activation was inhibited in Cxcr3 mice. Taken together, these data suggest that spinal CXCR3 mediates chronic itch and alloknesis, and targeting CXCR3 may provide effective treatment for chronic pruritus.
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Texto completo: 1 Base de datos: WPRIM Asunto principal: Dolor / Patología / Prurito / Pirimidinas / Piel / Médula Espinal / Factores de Tiempo / Cloroquina / Adyuvante de Freund / Enfermedad Crónica Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Neuroscience Bulletin Año: 2018 Tipo del documento: Article
Texto completo: 1 Base de datos: WPRIM Asunto principal: Dolor / Patología / Prurito / Pirimidinas / Piel / Médula Espinal / Factores de Tiempo / Cloroquina / Adyuvante de Freund / Enfermedad Crónica Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Neuroscience Bulletin Año: 2018 Tipo del documento: Article