MORPHINE SUPPRESSES THE PROESTROUS SURGE OF GnRH IN PITUITARY PORTAL PLASMA OF RATS

Ching, Melvin

doi:10.1210/endo-112-6-2209

Cited by 102 publications

(34 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Our results extend the findings of several recent studies on the consequent changes in GnRH secretion during naloxone treatment in rats and rabbits. In anaesthetized stalk-sectioned rats morphine decreased the magnitude of the pro-oestrous surge (Ching, 1983) and naloxone increased the mean portal concentrations of GnRH in male rats (Blank et al, 1985). Since in both of these studies the pituitary stalk was transected, concomitant measurements of LH secretion were not possible, as they were in the present study.…”

Section: Discussionmentioning

confidence: 66%

“…In vivo, naloxone increases (Blank et al, 1985) GnRH secretion in male rats and morphine suppresses (Ching, 1983) the preovulatory GnRH surge in the hypophysial portal blood of anaes¬ thetized rats, but concomitant LH measurements were not possible because the animals were stalksectioned to obtain the samples. The present study was undertaken to determine whether naloxone affects pituitary LH secretion via an effect on GnRH secretion in the conscious ewe.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Naloxone evokes large-amplitude GnRH pulses in luteal-phase ewes

Horton¹,

Cummins²,

Clarke³

1987

Reproduction

View full text Add to dashboard Cite

Summary. Ewes were sampled during the mid-late luteal phase of the oestrous cycle. Hypophysial portal and jugular venous blood samples were collected at 5\p=n-\10min intervals for a minimum of 3 h, before i.v. infusions of saline (12 ml/h; N = 6) or naloxone (40 mg/h; N = 6) for 2 h. During the 2-h saline infusion 2/6 sheep exhibited a GnRH/LH pulse; 3/6 saline infused ewes did not show a pulse during the 6\p=n-\8-hportal blood sampling period. In contrast, large amplitude GnRH/LH pulses were observed during naloxone treatment in 5/6 ewes. The mean ( \ m=+-\ s.e.m.) amplitude of the LH secretory episodes during the naloxone infusion (1\m=.\07\ m=+-\ 0\m=.\11ng/ml) was significantly (P < 0\m=.\05) greater than that before the infusion in the same sheep (0\m=.\54 \ m=+-\0\m=.\15 ng/ml). Naloxone significantly (P < 0\m=.\005) increased the mean GnRH pulse amplitude in the 5/6 responding ewes from a pre-infusion value of 0\m=.\99\ m=+-\ 0\m=.\22pg/min to 4\m=.\39\ m=+-\1\m=.\10pg/min during infusion. This episodic GnRH secretory rate during naloxone treatment was also significantly (P < 0\m=.\05)greater than in the saline-infused sheep (1\m=.\53 \m=+-\0\m=.\28 pg/min). Plasma FSH and prolactin concentrations did not change in response to the opiate antagonist.Perturbation of the endogenous opioid peptide system in the ewe by naloxone therefore increases the secretion of hypothalamic GnRH into the hypophysial portal vasculature. The response is characterized by a large-amplitude GnRH pulse which, in turn, causes a large-amplitude pulse of LH to be released by the pituitary gland.

show abstract

Section: Discussionmentioning

confidence: 66%

Section: Introductionmentioning

confidence: 99%

Naloxone evokes large-amplitude GnRH pulses in luteal-phase ewes

Horton¹,

Cummins²,

Clarke³

1987

Reproduction

View full text Add to dashboard Cite

show abstract

“…There is considerable evidence that endogenous opioid peptides tonically inhibit POA GnRH neurons in rats. Chronic treatment with morphine blocked GnRH secretion (42) and decreased POA GnRH mRNA levels (133), whereas the opioid receptor antagonist naloxone increased plasma LH levels and POA GnRH mRNA levels. Several studies suggest that endogenous opioids inhibit LH secretion in rabbits (163,250), ferrets (120), and cats (101).…”

Section: Opioid Peptidesmentioning

confidence: 93%

Neuroendocrine Regulation of GnRH Release in Induced Ovulators

Bakker

Baum

2000

Frontiers in Neuroendocrinology

180

135

View full text Add to dashboard Cite

GnRH is the key neuropeptide controlling reproductive function in all vertebrate species. Two different neuroendocrine mechanisms have evolved among female mammals to regulate the mediobasal hypothalamic (MBH) release of GnRH leading to the preovulatory secretion of LH by the anterior pituitary gland. In females of spontaneously ovulating species, including rats, mice, guinea pigs, sheep, monkeys, and women, ovarian steroids secreted by maturing ovarian follicles induce a pulsatile pattern of GnRH release in the median eminence that, in turn, stimulates a preovulatory LH surge. In females of induced ovulating species, including rabbits, ferrets, cats, and camels, the preovulatory release of GnRH, and the resultant preovulatory LH surge, is induced by the receipt of genital somatosensory stimuli during mating. Induced ovulators generally do not show "spontaneous" steroid-induced LH surges during their reproductive cycles, suggesting that the positive feedback actions of steroid hormones on GnRH release are reduced or absent in these species. By contrast, mating-induced preovulatory surges occasionally occur in some spontaneously ovulating species. Most research in the field of GnRH neurobiology has been performed using spontaneous ovulators including rat, guinea pig, sheep, and rhesus monkey. This review summarizes the literature concerning the neuroendocrine mechanisms controlling GnRH biosynthesis and release in females of several induced ovulating species, and whenever possible it contrasts the results with those obtained for spontaneously ovulating species. It also considers the adaptive, evolutionary benefits and disadvantages of each type of ovulatory control mechanism. In females of induced ovulating species estradiol acts in the brain to induce aspects of proceptive and receptive sexual behavior. The primary mechanism involved in the preovulatory release of GnRH among induced ovulators involves the activation of midbrain and brainstem noradrenergic neurons in response to genital-somatosensory signals generated by receipt of an intromission from a male during mating. These noradrenergic neurons project to the MBH and, when activated, promote the release of GnRH from nerve terminals in the median eminence. In contrast to spontaneous ovulators, there is little evidence that endogenous opioid peptides normally inhibit MBH GnRH release among induced ovulators. Instead, the neural signals that induce a preovulatory LH surge in these species seem to be primarily excitatory. A complete understanding of the neuroendocrine control of ovulation will only be achieved in the future by comparative studies of several animal model systems in which mating-induced as well as spontaneous, hormonally stimulated activation of GnRH neurons drives the preovulatory LH surge. KEY WORDS: GnRH; MBH; induced ovulators; neuroendocrine regulation; preovulatory LH surge; spontaneous ovulators. © 2000 Academic Press Address correspondence and reprint requests to M. J. Baum at Dept. Biology, Boston University, 5 Cummington Street, Boston...

show abstract

“…Opioids may inhibit LH secretion by suppressing hypothalamic discharge of gonadotrophin-releasing hormone (GnRH; Wilkes & Yen, 1981;Blank & Roberts, 1982;Ching, 1983;Rasmussen et ai, 1989). Pituitary responsiveness to an exogenous challenge of GnRH is unaltered in animals treated with opioid agonists or antagonists (Cicero et ai, 1980;Ferin et ai, 1984).…”

Section: Introductionmentioning

confidence: 99%

Opioid modulation of LH secretion by pig pituitary cells in vitro

Barb

Barrett²,

Wright³

et al. 1990

Reproduction

View full text Add to dashboard Cite

Summary. The effects of naloxone and \g=b\-endorphin on LH secretion by pig pituitary cells were studied in primary cultures. On Day 4 of culture, cells (105 seeded/well) were challenged with 10\m=-\9, 10\ m=-\ 8 or 10\ m=-\ 7 m gonadotrophin-releasing hormone (GnRH), 10\m=-\10,10\m=-\9, 10\m=-\8 or 10\m=-\7 m-\g=b\-endorphin or 10\m=-\6 m-naloxone individually or in combinations. Secreted LH was measured at 4 h and 24 h after treatment and cellular content of LH was measured after 24 h. Basal LH secretion (control) was 23\m=.\5\ m=+-\7\m=.\6and 36\m=.\9 \m=+-\ 10\m=.\3 ng/well at 4h and 24 h, respectively. Relative to control at 4h, 10\m=-\9, 10\m=-\8 or 1 0 \ m = -\ 7 m-GnRH stimulated (P < 0\m=.\05) LH secretion 140%, 210% and 250%, respectively. At 24h, LH secretion was increased (P < 0\m=.\05)by GnRH compared to control, but the does\p=n-\response to GnRH was absent. Naloxone increased (P < 0\m=.\01) LH secretion 166 \ m=+-\ 13% at 4h and 141 \m=+-\ 13% (P < 0\m=.\06) at 24h. Secretion of LH after simultaneous addition of 10\ m=-\ 8 m-GnRH plus naloxone was greater (P < 0\m=.\01) than after GnRH alone at 4h but not at 24h. \g=b\-Endorphin at 10\ m=-\ 10, 10\ m=-\ 9, 1 0 \ m= -\ 8

show abstract

MORPHINE SUPPRESSES THE PROESTROUS SURGE OF GnRH IN PITUITARY PORTAL PLASMA OF RATS

Cited by 102 publications

References 7 publications

Naloxone evokes large-amplitude GnRH pulses in luteal-phase ewes

Naloxone evokes large-amplitude GnRH pulses in luteal-phase ewes

Neuroendocrine Regulation of GnRH Release in Induced Ovulators

Opioid modulation of LH secretion by pig pituitary cells in vitro

Contact Info

Product

Resources

About