Chan, Stella Sze WaStella Sze WaChanLu, ZengbingZengbingLuLin, G.Yew, D. T. W.Yeung, C. K.Rudd, J. A.2023-06-192023-06-192014https://repository.sfu.edu.hk/handle/sfu/4038The use of glucagon-like peptide-1 (7–36) amide (GLP-1) receptor agonists for the treatment of type 2 diabetes mellitus is commonly associated with nausea and vomiting. Previous studies using Suncus murinus revealed that the GLP-1 receptor agonist, exendin-4, induces emesis via the brainstem and/or hypothalamus. The present study investigated the mechanism of exendin-4-induced emesis in more detail. Ondansetron (1 mg/kg, s.c.) and CP-99,994 (10 mg/kg, s.c) failed to reduce emesis induced by exendin-4 (3 nmol, i.c.v.), suggesting that 5-HT₃ and NK₁ receptors are not involved in the mechanism. In other studies, the GLP-1 receptor antagonist, exendin (9–39), antagonised emesis and c-Fos expression in the brainstem and the paraventricular hypothalamus induced by the chemotherapeutic drug cisplatin (30 mg/kg, i.p.; p < 0.05), but not the emesis induced by nicotine (5 mg/kg, s.c.; p > 0.05), or copper sulphate pentahydrate (120 mg/kg, p.o.; p > 0.05). GLP-1 receptors may therefore represent a potential target for drugs to prevent chemotherapy-induced emesis in situations where 5-HT₃ and NK₁ receptor antagonists fail.enjournal article10.1016/j.neuropharm.2014.03.016