title: Prolactin suppresses GnRH but not TSH secretion.
abstract: OBJECTIVE
  In animal models, prolactin increases tuberoinfundibular dopamine turnover, which has been demonstrated to suppress both hypothalamic GnRH and pituitary TSH secretion. To test the hypothesis that prolactin suppresses GnRH and TSH secretion in women, as preliminary evidence that a short-feedback dopamine loop also operates in the human, the effect of hyperprolactinemia on GnRH and TSH secretion was examined.
  
  
  METHODS
  Subjects (n=6) underwent blood sampling every 10 min in the follicular phase of a control cycle and during a 12-hour recombinant human prolactin (r-hPRL) infusion preceded by 7 days of twice-daily subcutaneous r-hPRL injections. LH and TSH pulse patterns and menstrual cycle parameters were measured.
  
  
  RESULTS
  During the 7 days of r-hPRL administration, baseline prolactin increased from 16.0+/-3.0 to 101.6+/-11.6 microg/l, with a further increase to 253.7+/-27.7 microg/l during the 12-hour infusion. LH pulse frequency decreased (8.7+/-1.0 to 6.0+/-1.0 pulses/12 h; p<0.05) with r-hPRL administration, but there were no changes in LH pulse amplitude or mean LH levels. There were also no changes in TSH pulse frequency, mean or peak TSH. The decreased LH pulse frequency did not affect estradiol, inhibin A or B concentrations, or menstrual cycle length.
  
  
  CONCLUSIONS
  These studies demonstrate that hyperprolactinemia suppresses pulsatile LH secretion but not TSH secretion and suggest that GnRH secretion is sensitive to hyperprolactinemia, but that TSH secretion is not. These data further suggest that the degree of GnRH disruption after 7 days of hyperprolactinemia is insufficient to disrupt menstrual cyclicity.
authors.affiliation: Reproductive Endocrine Unit, Department of Medicine, Massachusetts General Hospital, and Harvard Medical School, Boston, MA 02114, USA.
authors.forename: G
authors.initials: G
authors.lastname: Page-Wilson
authors.forename: P C
authors.initials: PC
authors.lastname: Smith
authors.forename: C K
authors.initials: CK
authors.lastname: Welt
mesh_terms: D000328:Adult; D004958:Estradiol / Q000097:blood / Q000502:physiology; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood / Q000502:physiology; D007987:Gonadotropin-Releasing Hormone / Q000037:antagonists & inhibitors / Q000097:blood / Q000378:metabolism*; D006801:Humans; D006966:Hyperprolactinemia / Q000097:blood / Q000503:physiopathology*; D007265:Inhibins / Q000097:blood / Q000502:physiology; D007986:Luteinizing Hormone / Q000097:blood / Q000378:metabolism; D008597:Menstrual Cycle / Q000502:physiology; D011374:Progesterone / Q000097:blood / Q000502:physiology; D011388:Prolactin / Q000378:metabolism / Q000494:pharmacology*; D011994:Recombinant Proteins / Q000494:pharmacology; D013972:Thyrotropin / Q000037:antagonists & inhibitors / Q000097:blood / Q000378:metabolism*
chemical_list: D011994:Recombinant Proteins; C422362:inhibin A; C422364:inhibin B; D007987:Gonadotropin-Releasing Hormone; D011374:Progesterone; D004958:Estradiol; D007265:Inhibins; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D013972:Thyrotropin