Opioid modulation of prolactin secretion induced by stress during late

VALDEZ SR; PENNACCHIO GE; GAMBOA DF; EG DE DINASSO; BREGONZIO C; SOAJE M

PHARMACOLOGICAL REPORTS

POLISH ACAD SCIENCES INST PHARMACOLOGY

Lugar: Polonia; Año: 2014 vol. 66 p. 383 - 396

1734-1140

Background: The opioid system modulates prolactin release during late pregnancy. Its role and theparticipation of ovarian hormones in this modulation are explored in ether stress-induced prolactinrelease.The opioid system modulates prolactin release during late pregnancy. Its role and theparticipation of ovarian hormones in this modulation are explored in ether stress-induced prolactinrelease.Methods/Results: Estrous, 3-day and 19-day pregnant rats were used. We administered the antagonistmifepristone (Mp) and tamoxifen to evaluate progesterone and estradiol action in naloxone (NAL, opioidantagonist) or saline treated rats. Ether stress had no effect on serum prolactin levels in controls butincreased prolactin release in NAL-treated rats. Prolactin response to stress in NAL-treated rats wasblocked by L-DOPA administration. Mp treatment on day 18 of pregnancy increased prolactin levels afterstress without alterations by NAL. Tamoxifen on days 14 and 15 of pregnancy completely blocked Mpand NAL effects on prolactin release at late pregnancy. In contrast, stress significantly increased prolactinlevels in estrous rats and pretreatment with NAL prevented this. On day 3 of pregnancy, at 6.00 p.m.,stress and NAL treatment inhibited prolactin levels in saline-treated rat. No effect of stress or NALadministration was detected on day 3 of pregnancy at 9.00 a.m. icv administration of specific opioidsantagonist, B-Funaltrexamine but not Nor-Binaltorphimine or Naltrindole, caused a significant increasein stress-induced prolactin release.Estrous, 3-day and 19-day pregnant rats were used. We administered the antagonistmifepristone (Mp) and tamoxifen to evaluate progesterone and estradiol action in naloxone (NAL, opioidantagonist) or saline treated rats. Ether stress had no effect on serum prolactin levels in controls butincreased prolactin release in NAL-treated rats. Prolactin response to stress in NAL-treated rats wasblocked by L-DOPA administration. Mp treatment on day 18 of pregnancy increased prolactin levels afterstress without alterations by NAL. Tamoxifen on days 14 and 15 of pregnancy completely blocked Mpand NAL effects on prolactin release at late pregnancy. In contrast, stress significantly increased prolactinlevels in estrous rats and pretreatment with NAL prevented this. On day 3 of pregnancy, at 6.00 p.m.,stress and NAL treatment inhibited prolactin levels in saline-treated rat. No effect of stress or NALadministration was detected on day 3 of pregnancy at 9.00 a.m. icv administration of specific opioidsantagonist, B-Funaltrexamine but not Nor-Binaltorphimine or Naltrindole, caused a significant increasein stress-induced prolactin release.L-DOPA administration. Mp treatment on day 18 of pregnancy increased prolactin levels afterstress without alterations by NAL. Tamoxifen on days 14 and 15 of pregnancy completely blocked Mpand NAL effects on prolactin release at late pregnancy. In contrast, stress significantly increased prolactinlevels in estrous rats and pretreatment with NAL prevented this. On day 3 of pregnancy, at 6.00 p.m.,stress and NAL treatment inhibited prolactin levels in saline-treated rat. No effect of stress or NALadministration was detected on day 3 of pregnancy at 9.00 a.m. icv administration of specific opioidsantagonist, B-Funaltrexamine but not Nor-Binaltorphimine or Naltrindole, caused a significant increasein stress-induced prolactin release.icv administration of specific opioidsantagonist, B-Funaltrexamine but not Nor-Binaltorphimine or Naltrindole, caused a significant increasein stress-induced prolactin release.Conclusions: Opioid system suppression of prolactin stress response during late pregnancy was observedonly after progesterone withdrawal, involving a different opioid mechanism from its well-establishedstimulatory role. This mechanism acts through a mu opioid receptor and requires estrogen participation.The opioid system and progesterone may modulate stress-induced prolactin release, probably involvinga putative prolactin-releasing factor.Opioid system suppression of prolactin stress response during late pregnancy was observedonly after progesterone withdrawal, involving a different opioid mechanism from its well-establishedstimulatory role. This mechanism acts through a mu opioid receptor and requires estrogen participation.The opioid system and progesterone may modulate stress-induced prolactin release, probably involvinga putative prolactin-releasing factor.