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

Kyungyoon Kam, Yongbin Park, Minseok Cheon, Gi Hoon Son, Kyungjin Kim, Kyungza Ryu

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31 Citations (Scopus)

Abstract

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 (E 2) in ovariectomized rats. Two weeks after bilateral ovariectomy, animals were implanted with the capsule containing E 2 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 E 2-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 E 2-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, E 2-treated group. Dopamine D2 receptor mRNA levels in the anterior pituitary of OVX, E 2-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, E 2-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, E 2-treated rats when determined at 1800 h. Therefore, we concluded that immobilization stress blocks E 2-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 E 2- induced PRL surge.

Original languageEnglish
Pages (from-to)279-287
Number of pages9
JournalEndocrine
Volume12
Issue number3
Publication statusPublished - 2000 Jul 15

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Keywords

  • Dopamine D2 receptor
  • Gonadotropin- releasing hormone
  • Gonadotropin-releasing hormone receptor
  • Immobilization stress
  • Luteinizing hormone
  • Prolactin

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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