Opioid modulation of FSH, growth hormone and prolactin secretion in the prepuberal gilt

Publisher Website
Google Scholar
Abstract
The role of endogenous opioid peptides (EOP) in modulating GH, prolactin (PRL) and FSH secretion was evaluated in prepuberal (P) gilts. In experiment I, P gilts received 1 (n = 2), 3 (n = 3) or 6 (n = 3) mg naloxone (NAL)/kg body weight i.v. Blood was collected every 15 min for 2 h prior to and 2 h after NAL and an additional 1 h after 100 μg gonadotrophinreleasing hormone (GnRH) i.v. In experiment II, P and mature (M) gilts were ovariectomized. Three weeks after ovariectomy, P and M gilts were injected twice a day for 10 days with either 0·85 mg progesterone (P4)/kg body weight or oil vehicle (V), resulting in the following groups: PP4 (n=11), PV (n = 10), MP4 (n=11) and MV (n=10). All gilts received 1 mg NAL/kg body weight on the last day of treatment. Blood samples were collected every 15 min for 4 h before and 2 h after NAL and an additional 1 h after 100μg GnRH i.v. In experiment III, six P and five M gilts were ovariectomized and surgically implanted with intracerebroventricular (i.c.v.) cannulae. Blood was collected every 15 min for 3 h before and 3 h after i.c.v. injection of 500 μg morphine in artificial cerebrospinal fluid (CSF) or 250 μl CSF. In experiment I, all doses of NAL failed to alter PRL secretion, while NAL increased (PP PP 4 gilts. Serum PRL and FSH concentrations were unaltered by NAL in PV, PP4 and MV gilts. In experiment III, mean serum GH, PRL and FSH concentrations were unaffected by CSF injections. Morphine treatment evoked a rapid increase in serum GH and PRL concentrations in both P and M gilts. In contrast, morphine failed to influence FSH secretion in P gilts but did suppress FSH concentrations in M gilts. These data suggest that EOP receptors are functionally coupled to the GH and PRL secretory systems. There is an age-related change in EOP modulation of PRL secretion, while EOP modulation of FSH secretion is an age- and ovarian-dependent process. Journal of Endocrinology (1992) 133, 13–19

This publication has 0 references indexed in Scilit: