Relationship between anti-aversive effects of salmon calcitonin and plasma levels of ACTH, beta-endorphin and prostaglandin E2 in mice.
We investigated whether the anti-aversive effects of salmon calcitonin (SCT) was induced by increasing ACTH and beta-endorphin and/or by decreasing of prostaglandin E2 (PGE2) levels in plasma of mice to elucidate the mechanisms responsible for the analgesic effects of SCT. Intracerebroventricular (i.c.v.) injections of SCT inhibited acetic acid-induced aversive behavior (writhing) in a U-shaped dose response curve, the most effective dose being 0.1 IU/mouse. Intraperitoneal (i.p.) injections of acetic acid increased, but not significantly, the levels of plasma ACTH and PGE2, but not beta-endorphin, which are considered to be psychoneuroendocrines correlated with pain. SCT (0.1 IU/mouse, i.c.v.) significantly increased plasma ACTH levels (p < 0.05) and tended to increase beta-endorphin levels (p = 0.052) in acetic acid-treated mice, whereas no change in PGE2 level was observed (p > 0.1). These results suggest that the anti-aversive effects of SCT may be mediated, at least in part, by the activation of ACTH.
Maeda
Y
Y
Department of Neuropsychopharmacology, Nagoya University School of Medicine, Japan.
Yamada
K
K
Hasegawa
T
T
Kawamata
Y
Y
Uchida
K
K
Iyo
M
M
Fukui
S
S
Nabeshima
T
T
D000085:Acetates / Q000037:antagonists & inhibitors; D019342:Acetic Acid; D000324:Adrenocorticotropic Hormone / Q000097:blood*; D000700:Analgesics / Q000494:pharmacology*; D000818:Animals; D002116:Calcitonin / Q000494:pharmacology*; D015232:Dinoprostone / Q000097:blood*; D008297:Male; D051379:Mice; D010146:Pain / Q000139:chemically induced / Q000517:prevention & control; D011863:Radioimmunoassay; D001615:beta-Endorphin / Q000097:blood*
D000085:Acetates; D000700:Analgesics; D001615:beta-Endorphin; C028815:salmon calcitonin; D000324:Adrenocorticotropic Hormone; D002116:Calcitonin; D015232:Dinoprostone; D019342:Acetic Acid