Inhibitory effect of a new opioid agonist on reproductive endocrine activity in rats of both sexes

Markó, M.; Römer, D.

doi:10.1016/0024-3205(83)90381-8

Cited by 32 publications

(17 citation statements)

References 10 publications

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“…DYN, a k receptor agonist [4,44], was found to be more effective in suppressing LH release than stimulating PRL secretion. In fact another k receptor ago nist, bremazocine [29], selectively suppressed LH release in our study. Therefore, it would seem that DYN may nor mally suppress LH release by selective activation of k re ceptors in the brain.…”

Section: Discussionmentioning

confidence: 70%

“…To identify the opiate receptor subtype involved in EOP-induced LH and PRL responses, several opiate agonists were tested: the g receptor agonist MOR [|l-casomorphin ( I -4) amide] ]5], the 8 receptor agonist DRP (Tyr-D-Ser-Gly-Phe-Leu-Thr) [I I], and the k receptor agonist bremazocine [29], MOR (10 gg) and DRP (10 gg) were administered intraventricularly as described in experi ment I. Bremazocine is not soluble in saline; therefore, it was first dissolved in ethanol and then diluted to 10% ethanol in saline. Since 10% ethanol-saline administered intraventricularly was found to alter LH and PRL release (preliminary findings), brem azocine was injected intravenously in these experiments.…”

Section: Methodsmentioning

confidence: 99%

“…Therefore, in view of these differ ences and the current view that EOP may exert a tonic in hibitory influence on LH release [3,6,20,21], we have reas sessed the effects of various EOP and the synthetic analogs, FK-33824 and DALAMID [22,29,34], on LH release in long-term ovariectomized rats. In these studies, LH levels were monitored at 5-min intervals for 2 h after injection of the neuroactive substances into the third ventricle of the brain.…”

mentioning

confidence: 99%

“…Koeniget al [27] noted that stimulation of PRL secretion by morphine may be me diated by p receptors in intact male rats. In these studies we have assessed the effects of other opiate receptor agonists such as delta receptor peptide (DRP; 8 receptor agonist) [II], morphiceptin (MOR; p receptor agonist) [5], and hremazocine [k receptor agonist; 2-(l-hydroxy-cycloprophylmethyl)-5-elhyl-9,9-dimethyl-2'-hydroxy-6,7-benzomorphan] [29] in an attempt to identify the opiate receptor subtypes which may be involved in the regulation of LH and PRL secretion in ovariectomized rats.…”

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confidence: 99%

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Effects of Endogenous Opioid Peptides and Opiates on Luteinizing Hormone and Prolactin Secretion in Ovariectomized Rats

1985

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Adult female rats were implanted with permanent cannulae in the third ventricle of the brain and ovariectomized. 3 weeks later, blood samples were withdrawn every 5 min from intraatrial cannulae placed the previous day. After a control sampling period of 30 min, the rats received an intraventricular bolus injection of saline (2 µl) or β-endorphin (βE; 10 µg); sampling was continued for an additional 2 h. Saline injection caused no effect on luteinizing hormone (LH) and prolactin (PRL) secretion. βE stimulated PRL secretion within 5–10 min, the values peaked in the next 10 min. Thereafter, as PRL levels fell, a suppression of LH secretion became apparent. Inhibition of LH release started 20–35 min after βE injection and lasted for 35–65 min. The antecendent PRL secretion was apparently not responsible for the observed delayed LH response, since blockade of PRL response with bromocriptine failed to affect the βE-induced LH suppression. Further, continuous intraventricular infusion of βE (5 or 10 µg/h) for 3 h markedly suppressed the amplitude and frequency of LH episodes in long-term ovariectomized rats. Bolus intraventricular injection of other endogenous opioid peptides and opiate receptor agonists produced different PRL and LH responses. Dynorphin (10 µg) similarly suppressed LH release but was only moderately effective in stimulating PRL. Leucine enkephalin (50 µg) stimulated LH and inhibited PRL release, while methionine-enkephalin (50 µg) selectively stimulated PRL release. The methionine-enkephalin analogs, FK-33824 (50 ng) and DALAMID (50 µg), evoked sequential PRL and LH responses similar to those seen after βE injection. Interestingly, morphiceptin (a specific µ receptor agonist; 10 µg) markedly suppressed LH release, but only sparingly stimulated PRL release. Delta receptor peptide (a specific δ receptor agonist; 10 µg) selectively suppressed LH release. Bremazocine (a specific Kreceptor agonist; 0.5 mg/kg) administered intravenously suppressed LH release selectively. These studies show that (1) of the four endogenous opioid peptides tested βE was most effective in evoking sequential PRL and LH responses, and these effects may be mediated by either Ε receptors or multiple opiate receptor subtypes; (2) stimulation of Kreceptors by bynorphin or bremazocine suppressed LH release, and (3) further studies would be needed to unterstand the mode of action of the two enkephalins and the δ opiate receptors in eliciting disparate PRL and LH responses.

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Section: Discussionmentioning

confidence: 70%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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confidence: 99%

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Effects of Endogenous Opioid Peptides and Opiates on Luteinizing Hormone and Prolactin Secretion in Ovariectomized Rats

1985

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“…Studies of opiate receptor subtype involvement in the regulation of LH release, employing specific agonists or antagonists for mu-, delta-or kappa-receptors, have been reported. Although some experiments employing agonist compounds in ovariectomized rats have indicated that opioid regulation of LH secretion involves mu-receptors only (14, 1 3 , other studies in ovariectomized (1 3, 16, 17) and adult female (16) rats, or prepubertal (18) and adult male (16,18) rats, have clearly shown that activation of not only mu-, but also kappa-and delta-opioid receptors, can decrease LH release. In studies involving antagonists of specific opioid receptors, blockade of mu-receptors with B-FNA increased LH release in the castrated male rat (19), and although effective in blocking the decrease in LH release produced by mu opiate agonists (15), had no effect on control plasma LH levels (1 5, 20) in ovariectomized rats.…”

Section: Discussionmentioning

confidence: 99%

Kappa‐Opioid Receptor Involvement in the Regulation of Pulsatile Luteinizing Hormone Release During Early Pregnancy in the Rat

Gallo

1990

J Neuroendocrinology

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The object of this study was to gain further insight into endogenous opioid peptide suppression of pulsatile luteinizing hormone (LH) release in early gestation in the rat by examining whether selective blockade of mu-, delta-, or kappa-opioid receptor(s) results in stimulation of pulsatile LH secretion at this time. Previous reports demonstrated stimulation of pulsatile LH release during early gestation by intravenous infusions of naloxone, an endogenous opioid peptide receptor antagonist whose binding is not specific to a single class of opioid peptide receptors. In the present study, naloxone infused intraventricularly similarly stimulated an increase in pulsatile LH release on Days 7 to 8 of gestation. Antagonists of specific opioid peptide receptor subtypes were thus given by this route. Administration of nor-binaltorphimine, an antagonist of kappa-opioid receptors, but not P-funaltrexamine or ICI 174, 864, antagonists of mu-and delta-opioid receptors, respectively, exerted a stimulatory action on both LH pulse amplitude and frequency similar to that of naloxone, indicating involvement of this opioid peptide receptor subtype in the endogenous opioid peptide suppression of pulsatile LH release in early gestation in the rat.Luteinizing hormone (LH) release is pulsatile during early pregnancy in the rat (1-3). The secretion of this hormone is important for maintenance of the corpus luteum, and therefore pregnancy, on Days 7 to 8 of gestation (4-10). Administration of naloxone, an endogenous opioid peptide (EOP) receptor antagonist, incieases LH pulse amplitude and frequency at this stage of pregnancy (2, 3), and this stimulatory effect is not exerted at the pituitary level (2). This latter study demonstrated that EOPs exert a suppressive action on pulsatile LH release during early pregniincy in the rat. However, the binding of naloxone is not specific to one class (i.e. mu, delta or kappa) of opioid peptide receptors (1 1-13). Thus, the objective of this study was to gain further imight into EOP regulation of LH pulse amplitude and frequency in early gestation, by examining whether selective blockade of mu-, delta-or kappa-opioid receptor(s) results in stimulation of pulsatile LH release at this time. Results E.lperiment IBasal pulsatile LH release in rats receiving a 4-h intraventricular infusion of artificial cerebrospinal fluid (CSF) was similar to that previously observed in early gestation in rats receiving a prolonged iv infusion of saline ( Fig. 1; 2, 3). In addition, naloxone given intraventricularly stimulated all three parameters of pulsatile LH secretion (Fig. 1) in a manner similar to that previously observed in response to iv naloxone infusion (2, 3). Thus, blockade of central EOP receptors can be elicited by intraventricular administration of naloxone. Moreover, these data demonstrate that implantation of cannulae in the third ventricle, together with brief ether exposure and intraventricular infusion on the day of the experiment, have no untoward effect on either basal or naloxone-stimul...

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Central Actions of Opiates and Opioid Peptides

Wood¹,

Iyengar²

1988

The Opiate Receptors

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Inhibitory effect of a new opioid agonist on reproductive endocrine activity in rats of both sexes

Cited by 32 publications

References 10 publications

Effects of Endogenous Opioid Peptides and Opiates on Luteinizing Hormone and Prolactin Secretion in Ovariectomized Rats

Effects of Endogenous Opioid Peptides and Opiates on Luteinizing Hormone and Prolactin Secretion in Ovariectomized Rats

Kappa‐Opioid Receptor Involvement in the Regulation of Pulsatile Luteinizing Hormone Release During Early Pregnancy in the Rat

Central Actions of Opiates and Opioid Peptides

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