Oral gavage of capsaicin causes TRPV1-dependent acute hypothermia and TRPV1-independent long-lasting increase of locomotor activity in the mouse.

摘要: Capsaicin (CAP), the pungent ingredient of hot red pepper, is a selective ligand for heat-sensitive transient receptor potential V1 cation channel 1 (TRPV1). Although CAP has been traditionally used as spices various foods in world, effect oral intake on thermoregulation and locomotor activity, CAP-induced activation brain neural circuits are not well understood. In this study, therefore, we examined effects gavage core body tail surface temperature, Fos expression thermoregulation- sensory information-associated hypothalamic medullary regions using freely moving mice. Oral acutely decreased temperature alternatively increased wild type (WT) mice, whereas such acute changes were observed TRPV1 knockout (KO) animals. Moreover, long-lasting increase activity was both WT KO mice after CAP, but seen only induced neuronal circumventricular organs, median medial preoptic area, arcuate nucleus, nucleus solitary tract, scarcely Thus, present study demonstrates that causes TRPV1-dependent hypothermia TRPV1-independent moreover activates controlling metabolism.