Effects of immobilization stress on estrogen-induced surges of luteinizing hormone and prolactin in ovariectomized rats

Reproductive function has been known to be impaired by various kinds of physical and emotional stress, but the mechanism by which stress impairs the reproductive axis has not been dearly understood. In the present study, the effects of immobilization stress were studied on the surges of luteinizing hormone (LH) and prolactin (PRL) induced by 17β-estradiol (E₂) in ovariectomized rats. Two weeks after bilateral ovariectomy, animals were implanted with the capsule containing E₂ or vehicle at 1000 h (designated as d 0). Immobilization was started at 1000 h and continued to 2100 h on d 2. Blood samples were collected according to the time schedule by a jugular vein catheter procedure. Immobilization stress inhibited basal release of LH and abolished E₂-induced LH and PRL surges in ovariectomized (OVX) rats. Daily repeated immobilization (from 1200 h to 1800 h, 6 h/d) for 3 d also abolished LH and PRL surges when examined at 1800 h on d 2. Although daily repeated immobilization stress reduced E₂-induced PRL mRNA levels, this stress failed to change LHβ mRNA levels in the anterior pituitary as determined by Northern blot analysis. Gonadotropin-releasing hormone (GnRH) receptor mRNA levels in the anterior pituitary were lowered by immobilization stress in the OVX, E₂-treated group. Dopamine D2 receptor mRNA levels in the anterior pituitary of OVX, E₂-treated rats were significantly decreased at 1800 h, compared with those at 1000 h. However, immobilization prevented a decrease in dopamine D2 receptor mRNA levels at 1800 h. GnRH content was increased in the mediobasal hypothalamus by immobilization in the OVX, E₂-treated group, suggesting that GnRH release was inhibited. Interestingly, GnRH mRNA levels in the preoptic area-anterior hypothalamic area were suppressed by immobilization stress in OVX, E₂-treated rats when determined at 1800 h. Therefore, we concluded that immobilization stress blocks E₂-induced LH surge possibly by inhibiting synthesis and release of GnRH at the hypothalamic level, and an increase of dopaminergic activity via D2 receptor at the pituitary level might be involved in the stress blockage of E₂- induced PRL surge.