抄録
It is well known that the limbic system and the hypothalamo-pituitary-adrenocortical (HPA) axis is activated in response to stressful stimuli in rats. In addition, estrogen enhances the stress responses in the female rat, but it remains unknown how estrogen affects stress responses. In the present study, we examined the possible pathway of estrogen affecting stress reponses. Adult female rats of Wistar-imamichi strain were ovariectomized 2 weeks prior to the experiment. The stainless steel tube containing cholesterol (Chol) or 17β-estradiol (E2) (Chol : E2 = 100 : 1 by weight) was stereotaxically implanted in the paraventricular nucleus (PVN) or the amygdala. Three days after the implantation, blood samples (300 μl) were taken every 1 h through an indwelling cardiac catheter from 1100 h to 1600 h to monitor the serum corticosterone (CS) concentration as a marker of HPA axis activity, and restraint stress was applied from 1200 h to 1300 h. The serum CS concentration was assayed by a radioimmunoassay. The serum CS concentration increased at the onset of restraint, and gradually decreased after the release from the restraint in all experimental groups. E2 implantation in the amygdala caused a significant enhancement of the CS release response during the restaint, comparing Chol. On the other hand, no significant difference was observed between the two groups implanted with E2 or Chol in the PVN. The implantation did not affect the vaginal smear and the serum E2 concentration. These results suggest that amygdala is the possible pathway of E2 enhancing stress responses. [J Physiol Sci. 2006;56 Suppl:S218]
