Estrogen regulates GFAP-expression in specific subnuclei of the female rat interpeduncular nucleus: a potential role for estrogen receptor beta.
Estrogen regulates GFAP-expression in specific subnuclei of the female rat interpeduncular nucleus: a potential role for estrogen receptor beta.
复制标题
雌激素调节雌性大鼠脚间核特定亚核中的 GFAP 表达:雌激素受体 β 的潜在作用。
DOI:
10.1016/s0006-8993(02)03771-x
复制
发表时间:
2002
期刊:
影响因子:
2.9
通讯作者:
Belcher,ScottM
中科院分区:
文献类型:
--
作者:
Zsarnovszky,Attila;Smith,Todd;Hajos,Ferenc;Belcher,ScottM
We previously demonstrated that in rat, astrocytic glial fibrillary acidic protein- (GFAP) expression in the interpeduncular nucleus (IPN) was responsive to testosterone and in females the intensity of GFAP-immunoreactivity (IR) followed the periodic hormonal changes of the estrous cycle. The aim of this study was to test whether 17β-estradiol (E2), in the absence of other ovarian hormones, can influence GFAP-expression within individual subnuclei of the IPN and to determine the cellular distribution of estrogen receptor β (ERβ) in the IPN. Quantitative surface-density analysis was used to compare the intensity of GFAP-IR at different anterio-posterior (AP) levels of the IPN in ovariectomized female rats 24 h after treatment with E2or vehicle. Estrogen-treatment resulted in a significant increase in GFAP-IR in the rostrolateral subnucleus of the IPN at AP: −5.60, in the lateral-, dorsolateral-, dorsomedial- and central subnuclei at −6.04 and in the lateral subnucleus at −6.72. No significant differences were observed at −5.80 and −6.30. These results indicate that E2, in the absence of other ovarian hormones, modulates GFAP-expression within select IPN subnuclei and that these affects are dependent on position along the AP axis. To determine whether ERβ was a possible mediator of the observed estrogenic effects, adjacent section pairs of the IPN were immunostained for ERβ or GFAP. Using the ‘mirror’ method, ERβ-IR was detected in the cytoplasm of GFAP-immunopositive astroglia and in the nuclei of GFAP-immunonegative neurons. These findings suggest that in the IPN, E2may directly modulate GFAP-expression through ERβ-mediated mechanisms.