Image_1_Intradermal Injection of Oxytocin Aggravates Chloroquine-Induced Itch Responses via Activating the Vasopressin-1a Receptor/Nitric Oxide Pathwa.jpeg (95.96 kB)
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Image_1_Intradermal Injection of Oxytocin Aggravates Chloroquine-Induced Itch Responses via Activating the Vasopressin-1a Receptor/Nitric Oxide Pathway in Mice.jpeg

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posted on 2019-11-21, 10:55 authored by Rulong Li, Hua Sun, Haotian Zheng, Zhihua Zong, Shengnan Li, Tingting Meng, Jing Li, Yunfang Liu, Chao Wang, Jingxin Li

Oxytocin (OT), a hormone synthesized within the paraventricular nucleus and supraoptic nucleus of the hypothalamus, when given intracerebroventricularly, induces strong scratching behaviors. However, it is not clear whether intradermal injection (ID) of OT elicits itch sensation. Herein, we found that OT (0.02 mg/ml) did not elicit an itch-scratching response in mice but aggravated chloroquine (CQ, 3 mmol/L)-elicited scratching behavior. Similar to OT, arginine vasopressin (AVP, 0.02 mg/ml), which is structurally related to OT, also enhanced CQ-induced scratching behavior but did not directly induce scratching behavior in mice. Mechanistically, OT-mediated enhancement of CQ-induced scratching behavior was significantly suppressed by conivaptan (0.05 mg/ml), a vasopressin-1a receptor (V1AR) antagonist and 1,400 W (3 mg/kg), inhibitor of inducible nitric oxide synthase (iNOS), but not OT receptor (OTR) antagonist L-368,899 (0.05 mg/ml). Notably, conivaptan also directly decreased CQ-induced scratching. In conclusion, OT plays a role in CQ-induced scratching behavior via V1AR binding events. V1AR antagonists could be used as possible treatments for CQ-induced itch.

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