부산대학교 도서관

The purpose of this study was to evaluate the effects of stress and estradiol (E2) on pain tolerance. Ovari- ectomized rats were assigned to treatment groups based on a 2 x 4 factorial design comprising stress (nonstress x stress) and hormone treatment vehicle x E2 [0.25 mg/kg/d]) x estrogen receptor alpha (ERα)- selective agonist propyl pyrazole triol (1 mg/kg/d) x estrogen receptor beta (ERß)-selective agonist diaryl- propionitrile (1 mg/kg/d). Stressed animals underwent daily 60-minute immobilization for 22 days. Pain tolerance was assessed with the hot plate test, an acute thermal pain test. In this study, stressed rats showed increased (P < .05) pain tolerance compared with nonstressed rats (25.0 ± 1.92 s vs 20.4 ± 1.02 s, respectively). Increased (P < .05) pain threshold was observed in nonstressed and stressed rats treated with E2 and the ERα agonist compared with vehicle-treated rats. Interestingly, the ERß agonist only increased (P < .10) pain thresholds in stressed rats. Stressed rats exhibited higher (P < .05) ß-endorphin levels compared with nonstressed rats in all hormone- treatment groups. With the exception of stressed rats treated with the ERß agonist, there was no hormone effect on ß-endorphin levels. These studies suggest that E2's effect on pain thresholds may be mediated via the ERα, while the interaction between chronic stress and ERß may also enhance pain threshold. [ABSTRACT FROM AUTHOR]