INVESTIGADORES
BREGONZIO DIAZ Claudia
artículos
Título:
OPIOID MODULATION OF PROLACTIN SECRETION INDUCED BY STRESS DURING LATE PREGNANCY. ROLE OF OVARIAN STEROIDS
Autor/es:
VALDEZ, S; ; PENNACCHIO G.E; GAMBOA D.F; DI NASSO E.F; BREGONZIO C; SOAJE, M
Revista:
PHARMACOLOGICAL REPORTS
Editorial:
POLISH ACAD SCIENCES INST PHARMACOLOGY
Referencias:
Año: 2014
ISSN:
1734-1140
Resumen:
Background/Aims: The opioid system modulates prolactin release during late pregnancy. We explored its role in ether stress-induced prolactin release and the participation of ovarian hormones in this response. Methods/Results: Rats on day 19 of pregnancy were used. Ether exposure had no effect on serum prolactin levels in control but increased prolactin release in naloxone (NAL) treated rats. Prolactin response to stress in NAL-treated rats was blocked by L-DOPA administration. Mifepristone (Mp) treatment on day 18 of pregnancy induced an increase in prolactin levels after ether stress with no alterations by NAL. To compare prolactin response to stress in other reproductive states, oestrous rats and rats on day 3 of pregnancy were used. Ether stress induced a significant increase in prolactin levels in control oestrous rats and pretreatment with NAL prevented it. On day 3 of pregnancy at 18.00 h, ether stress and NAL treatment inhibited high prolactin levels observed in saline treated rats. No effect of ether stress or NAL administration was observed on day 3 of pregnancy at 09.00 h. The oestrogen receptor antagonist tamoxifen on days 14 and 15 of pregnancy completely blocked Mp and NAL effects. Administration i.c.v. of Beta-funaltrexamine, but not Nor-Binaltorphimine or Naltrindole, caused a significant increase in stress-induced prolactin release. Conclusions: The opioid system suppression of prolactin stress response during late pregnancy was observed only after progesterone withdrawal, maybe involving a different opioid mechanism from the stimulatory well established through µ-receptor requiring oestrogen. The opioid system and progesterone could modulate stress-induce prolactin release involving probably a putative prolactin-releasing factor.