Effects of Beta‐Endorphin on Pulsatile Luteinizing Hormone and Prolactin Secretion During the Follicular Phase in the Ewe

Abstract

The present study w a s undertaken to determine the effects of the endogenous opioid ligand 1-endorphin on pulsatile luteinizing hormone (LH) secretion and plasma prolactin concentrations during the follicular phase of the ewe. Oestrous cycles were synchronized by injection of prostaglandin analogue and, commencing 13 h later, saline or 1-endorphin (2, 10 or 50pg) was irilected intracerebroventricularly at hourly intervals for 3 h. Treatment with /%endorphin was followed by a significant reduction iii LH pulse frequency at all doses due to almost complete cessation of pulses. There were no significant changes in LH pulse amplitude or mean LH concentrations. At the lowest dose of ,&endorphin, LH pulses recommenced within 3 h of the last injection if; all animals and pulse frequency was not significantly different from the saline-injected controls during the 3 h post-treatment pcriod. Following treatment with 10 or 50 pg j-endorphin, LH pulse frequency remained suppressed during the 3 h post-treatment pt.riod but was not different from saline-treated controls on the following day. The time to the onset of the LH surge w a s not affected by intracerebroventricular j-endorphin. Plasma prolactin concentrations were significantly increased following intracerebroventricular injection of 10 or 50 pg 1-endorphin, declining to control values soon after treatments stopped. Intravenous administration of 50 pg j-endorphin had no effect on LH but w a s accompanied by a small increase in prolactin concentrations.While these results indicate that hypothalamic 8-endorphin may be involved in the central control of LH and prolactin secretion, they provide no evidence for subtle modulation of LH pulse frequency by this neuropeptide.St d i e s from a number of species have clearly demonstrated that tiic endogenous opioid peptides are potent inhibitors of luteinizing h>ii.mone (LH) secretion (1-3). However, much less is known ;I!)irut their role as physiological modulators of reproductive lu::iction. During the follicular phase of the oestrous cycle, subtle c!i.inges in LH pulse frequency and amplitude are likely to affect gi-owth and maturation of ovarian follicles which could be risllccted in parameters such as the ovulation rate. Opioid agonists ii id antagonists suppress and enhance follicular phase LH secre-[ i i u i , respectively (I), but there is little information on the effects 01 endogenous ligands such as 8-endorphin on pulsatile LH sccretion.The endogenous opioid peptides have also been implicated in the. control of prolactin secretion. Opioid agonists clearly stimu-1~1~ prolactin secretion in the rat (3); however in sheep, although nlorphine stimulates prolactin secretion (4), the mixed mu-and kappa-receptor agonist FD 33-824 has no effect suggesting that Prolactin secretion may be under different opioid control (5).The present study was undertaken to provide information on I h possible role of the endogenous opioid ligand j-endorphin in modulation of LH and prolactin secretion during the follicular phase. In p...

Beta-Endorphin Regulation of Luteinizing Hormone-Releasing Hormone Release at the Median Eminence in Ewes: Immunocytochemical and Physiological Evidence

“…It is well known that (LEND and other opiates inhibit LH release in ovines [1][2][3][4][5][6][7][8][9][10][11] and in other species [38,39]. There is also good evidence pointing to a hypothalamic site of action for this inhibitory effect [14,40].…”

“…In ewes, |3-endorphin ((3-END) has been implicated as an inhibitory component in the neuroendocrine control of luteinizing inhibitory component in the neuroendo crine control of luteinizing hormone (LH) release and thus, presumably, the hypophysiotropic luteinizing hor mone-releasing hormone (LHRH) release [1][2][3][4][5][6][7][8][9][10][11]. For example: (1) intracerebral immunoneutralization of [3-END disinhibits the release of LH [10]; (2) administra tion of P-END suppresses the amplitude and frequency of LH pulses while naloxone increases LH release [1,5,6,11], Stimulation of LH by naloxone constitutes one es sential criterion in establishing that LH release is being tonically inhibited by unidentified endogenous opiates (EOP); (3) hypothalamohypophyseal (portal) plasma concentration of (3-END is lower during the preovulatory surge of LH than 24 h before that event [3], and (4) im plants containing the EOP antagonist WIN 44,441-3 (WIN) in the medial preoptic area increase serum LH suggesting an EOP action at the area of LHRH cell bodies [11].…”

“…For example: (1) intracerebral immunoneutralization of [3-END disinhibits the release of LH [10]; (2) administra tion of P-END suppresses the amplitude and frequency of LH pulses while naloxone increases LH release [1,5,6,11], Stimulation of LH by naloxone constitutes one es sential criterion in establishing that LH release is being tonically inhibited by unidentified endogenous opiates (EOP); (3) hypothalamohypophyseal (portal) plasma concentration of (3-END is lower during the preovulatory surge of LH than 24 h before that event [3], and (4) im plants containing the EOP antagonist WIN 44,441-3 (WIN) in the medial preoptic area increase serum LH suggesting an EOP action at the area of LHRH cell bodies [11]. Although no functional evidence is yet avail able fora direct effect of (LEND on in vivo LHRH release by an action on LHRH terminals at the ME level, several lines of evidence suggest that (LEND may have an effect at the ME.…”

The role of GABA_A receptors in the neural systems of the medial preoptic area in the control of GnRH release during the luteal phase of the oestrous cycle in ewes

“…The presented results indicate that bicuculline reduced the tone of β-endorphinergic activity but did not increase GnRH release; such event is not strange because it is well documented that the inhibitory effects of β-endorphin on GnRH release are only marginally apparent in the luteal phase of the oestrous cycle in ewes (Conover et al, 1993). The inhibitory effect of β-endorphin on GnRH/LH release (Curlevis et al, 1991;Domański et al, 1991;Conover et al, 1993) as well as the stimulatory influence of naloxone (Conover et al, 1993) on GnRH secretion in the VEN/NI in ewes increases distinctly throughout the follicular phase reaching the highest value just prior to the preovulatory surge of gonadotropin. However, at the MPOA of ovariectomized-progesterone treated ewes the decrease of opioidergic activity by naltrexon suppressed the stimulatory influence of progesterone on GABA release and enhanced LH secretion (Tartonese, 1999).…”

The effects of <i>mu</i>-, <i>delta</i>- and <i>kappa</i>-opioid receptor activation on <i>in vitro</i> prolactin secretion by anterior pituitary cells of cyclic gilts

“…In other studies, neither naloxone nor mu-opioid receptor agonist, FK 33-824, affected plasma prolactin concentration in gilts at similar stage of the oestrous cycle (Okrasa et al, 1990). In turn, intracerebroventricular injections of β-endorphin significantly increased plasma prolactin concentrations in ewes during the early follicular phase (Curlewis et al, 1991). In the present in vitro study, during this stage of the cycle, opposing actions of opioid agonists on prolactin secretion by porcine pituitary cells, depending on the presence of TRH or dopamine, were observed.…”