Hideo Inoue (1), Nobuyuki Nagata (2) and Yasuko Koshihara (2)
(1) Research Laboratory, Minophagen Pharmaceutical Co., 2-5233, Komatsubara, Zama, Kanagawa 228, Japan
(2) Department of Biosignal Research, Tokyo Metropolitan Institute of Gerontology, Sakaecho, Itabashi-ku, Tokyo 173, Japan
Abstract: We investigated the involvement of serotonin (5-HT) in mouse ear edema induced by topical application of capsaicin (250 microg/ear). Application of capsaicin to the ear caused degranulation of mast cells in skin connective tissue. Capsaicin-induced ear edema was significantly inhibited by preadministration of 5-HT2 receptor antagonists such as ketanserin (2 mg/kg, i.v.) and LY 53857 (1 mg/kg, i.v.), but not 5-HT1-, 5-HT3- and 5-HT4-receptor antagonists. Intradermal injection of alpha-methyl 5-HT (5-HT2-receptor agonist) and 5-HT into ear skin produced edema formation more potently than 8-OH-DPAT (5-HT1A agonist) and 2-methyl 5-HT (5-HT3 agonist). 5-HT2 antagonists markedly suppressed the edema response to 5-HT and its receptor agonists, whereas any antagonist for 5-HT1, 5-HT3 and 5-HT4-receptors had no effect. Furthermore, 5-HT2-receptor antagonists partly prevented ear edema in response to substance P (SP), a putative mediator of capsaicin-induced edema, and compound 48/80, a releaser of vasoactive amines from mast cells. These results suggest that 5-HT released from mast cells is partly involved in the development of capsaicin-induced mouse ear edema via 5-HT2 receptors in the ear skin.
Keywords: Capsaicin, Serotonin (5-HT), Ear edema (mouse), 5-HT receptor, 5-HT-receptor antagonist
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