Seasonal and steroid-dependent effects on the modulation of LH secretion in the ewe by intracerebroventricularly administered β-endorphin or naloxone

Abstract

The natural opioid ligand, beta-endorphin, and the opioid antagonist, naloxone, were administered intracerebroventricularly (i.c.v.) to evaluate effects on LH secretion in ovariectomized ewes and in ovariectomized ewes treated with oestradiol-17 beta plus progesterone either during the breeding season or the anoestrous season. Ovary-intact ewes were also studied during the follicular phase of the oestrous cycle. Jugular blood samples were taken at 10-min intervals for 8 h and either saline (20-50 microliters), 100 micrograms naloxone or 10 micrograms beta-endorphin were injected i.c.v. after 4 h. In addition, luteal phase ewes were injected i.c.v. with 25 micrograms beta-endorphin(1-27), a purported endogenous opioid antagonist. In ovariectomized ewes, irrespective of season, saline and naloxone did not affect LH secretion, but beta-endorphin decreased the plasma LH concentrations, by reducing LH pulse frequency. The effect of beta-endorphin was blocked by administering naloxone 30 min beforehand. Treating ovariectomized ewes with oestradiol-17 beta plus progesterone during the breeding season reduced plasma LH concentrations from 6-8 micrograms/l to less than 1 microgram/l. In these ewes, saline did not alter LH secretion, but naloxone increased LH pulse frequency and the plasma concentrations of LH within 15-20 min. During anoestrus, the combination of oestradiol-17 beta plus progesterone to ovariectomized ewes reduced the plasma LH concentrations from 3-5 micrograms/l to undetectable levels, and neither saline nor naloxone affected LH secretion. During the follicular phase of the oestrous cycle, naloxone enhanced LH pulse frequency, which resulted in increased plasma LH concentrations; saline had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Melanocortins Mimic the Effects of Leptin to Restore Reproductive Function in Lean Hypogonadotropic Ewes

“…Groups received either naloxone (n = 5) or aCSF (n = 4) for 3 h by LV infusion in a crossover design. Since the response to naloxone is steroid-dependent [40], the experiment was replicated in OVX ewes with estradiol-17β and progesterone replacement to maximize the chance of an LH response. The former was administered by subcutaneous implantation of 3-cm implants inserted into the axillary region for 1 month and intravaginal progesterone delivery devices (CIDR: Riverina; Artificial Breeders Ltd., Albury, N.S.W., Australia) were inserted 2 days prior to the study.…”

“…The former was administered by subcutaneous implantation of 3-cm implants inserted into the axillary region for 1 month and intravaginal progesterone delivery devices (CIDR: Riverina; Artificial Breeders Ltd., Albury, N.S.W., Australia) were inserted 2 days prior to the study. Naloxone causes a transient response [40] which is limited to the 1st LH pulse following initiation of treatment. This was observed in the steroid-treated animals of normal body weight, and we repeated the experiment in lean animals (34.52 ± 0.60 kg) with and without sex steroid replacement.…”

The Influence of Photoperiod on the Hypothalamic Content of Beta‐Endorphin and the Luteinizing Hormone Responses to Naloxone and to Steroid Withdrawal in the Male Syrian Hamster

“…Restoration of the LH response to naloxonc indicated the return of endogenous opioidergic control over LH release coincidentally with reactivation of the gonadotrophic axis. It is well established that photoinhibition in hamsters and sheep is associated with the loss of the LH response to naloxone (19)(20)(21)(22)(23)(24), and in the pubertal male rat, a similar insensitivity to naloxone accompanies melatonin-induced delayed sexual maturation (29). Furthermore, in the sheep, a S D breeder, restoration of gonadal function in animals refractory to LD, is accompanied by renewed sensitivity to naloxone (20).…”

“…Following castration the response to naloxone is lost or severely attenuated, illustrating the close relationship between opioid and steroidal control of LH secretion (17)(18)(19)(20). The secretion of LH in photoinhibited animals, in which basal secretion of LH and testosterone are low, is also refractory to opiate blockade (13,20,21). However, the absence of a response in this case is not a result of the lower titres of steroid because it is not restored by the maintenance of high circulating levels of exogenous gonadal steroid (19)(20)(21)(22)(23)(24).…”

“…The secretion of LH in photoinhibited animals, in which basal secretion of LH and testosterone are low, is also refractory to opiate blockade (13,20,21). However, the absence of a response in this case is not a result of the lower titres of steroid because it is not restored by the maintenance of high circulating levels of exogenous gonadal steroid (19)(20)(21)(22)(23)(24). The profound effect of photoperiodic stimuli upon the activity of endogenous opioid systems, particularly their involvement in the release of gonadotrophin, raises the possibility that alterations of opioid activity may be a significant component of those neurocndocrine adjustments to photoperiod which determine reproductive status.…”