Association of Diurnal Variations in Hypothalamic but Not Cortical Opiate ([&lt;sup&gt;3&lt;/sup&gt;H]-Naloxone)-Binding Sites with the Ability of Naloxone to Induce LH Release in the Prepubertal Female Rat

Jacobson, W.; Wilkinson, Michael

doi:10.1159/000124634

Cited by 17 publications

(4 citation statements)

References 19 publications

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“…A similar sexual dimorphism has bccn demonstrated for opiate (37) and muscarinic rcccptors (38). Thus, the steroid environment and the time of day are two important factors in thc regulation of PGE, receptors, as they are for other receptors (39)(40)(41).…”

Section: Discussionsupporting

confidence: 52%

Circadian and Estral Changes in the Hypothalamic Prostaglandin E₂ Content and [³H]Prostaglandin E₂ Binding in Female Rats

Bommelaer-Bayet

Wisner

Renard

et al. 1990

J Neuroendocrinology

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Prostaglandin E, (PGE,) is involved in the luteinizing hormone-releasing hormone-stimulated luteinizing hormone surge in female rats and may act via specific membrane receptors. The following studies were performed to determine whether there were any changes in the hypothalamic PGE, binding and/or PGE, content which were specific to proestrus and not to the rest of the estrous cycle. Groups of female Wistar rats were sacrificed at 3-h intervals throughout the estrous cycle to determine both the circadian and circaestral changes in the hypothalamic PGE, content and [3H]PGE, binding. The hypothalamic PGE, content was maximal at 1700 h on each of the 4 consecutive days of the estrous cycle but was independent of the stage of the cycle.[3H]PGE, binding also displayed a circadian rhythm; the lowest binding occurred near the circadian peak of PGE,, suggesting that the PGE, binding sites were occupied by endogenous PGE,. Since such circadian rhythms were not observed in the hypothalamus of male rats, they may be under the control of ovarian steroids. Also, since PGE, binding and the PGE, content both exhibit a diurnal pattern independent of the day of the cycle, there may be changes in the PGE, receptor-mediated process coupled to an adenylyl cyclase which could explain the luteinizing hormone surge in proestrus.Prostaglandin E, (PGE,) induces the release of Iuteinizing hormone (LH) by stimulating luteinizing hormonc-rclcasing hormone (LHRH) release (1-5). There are also sevcral indications that PGs are involved in the modulation of LHRH release by steroids. The cyclo-oxygenase inhibitor, indomcthacin, prevents the steroidinduced release of gonadotrophin and lowcrs the elevated LH level of castrated animals (6). The preovulatory increase in PGE, synthesis, which precedes the LH surge, indicates that PGE, affects LH release in female rats (7,8), and a peak of PGE, release into the cerebrospinal fluid precedes the LH surge by 20 to 40 min (9). PGE, may act on LHRH release via specific membrane receptors (lo), since specific binding of [3H]PGE, to hypothalamic membranes is correlated with LHRH rclcase in vitro (1 1 ) .The preovulatory LH surge which occurs during proestrus in rats also requires a neural LHRH surge. This, in turn, depends upon adequate circulating titres of ovarian steroids (12). The effect of such a neurogenic stimulus was reported to be dependent on the time of day (1 3). In vitro PGE,-stimulated LHRH release from the median eminence (ME) also depcnds upon the stages of both the estrous and 24-h cycles (14). Such a change in M E sensitivity to PGE, could reflect a modification o f its PGE, binding capacity. However, LHRH release may be differently affected by PGE, and steroids, depending on the area of the hypothalamus: the comparative effect of norepinephrine (N E) on PGE, or LHRH release by the ME alone or hy the ME linkcd to the mediobasal hypothalamus (MBH/ME complex) suggests a regulation of the PGE,-stimulated LHRH release by neurons with cell body located in the MBH (15, 16). Moreover, thc...

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Section: Discussionsupporting

confidence: 52%

Circadian and Estral Changes in the Hypothalamic Prostaglandin E₂ Content and [³H]Prostaglandin E₂ Binding in Female Rats

Bommelaer-Bayet

Wisner

Renard

et al. 1990

J Neuroendocrinology

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“…Precedence for opioid receptor downregulation was provided by results in lactating rats, which were totally refractory to PRL stimulation by mor phine [47]. Moreover, the feasibility of opioid receptor downregulation occurring over short time periods is evi denced by a report showing a diurnal rhythm in the num ber of opioid receptors in immature female rats [48]. Finally, the concentration of PRL in the anterior pitu itary gland at any given time may affect the PRL response to exogenous P-End.…”

Section: Discussionmentioning

confidence: 99%

Time-Dependent Changes in β-Endorphin-Stimulated Prolactin Release during Pregnancy

Sagrillo¹,

Voogt²

1992

Neuroendocrinology

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Endogenous opioid peptides (EOPs) stimulate prolactin (PRL) release in various physiological conditions in the rat. Moreover, EOPs are essential in initiating and maintaining the nocturnal PRL surges that occur over the first half of gestation in the rat. The purpose of this study was to investigate the potential role of the opioid β-endorphin (β-End) in mediating the nocturnal PRL surges. Day 8 pregnant rats received an infusion of 2.5, 10, 25 or 100 ng/µl/min β-End intracerebroventricularly (i.c.v.) for 15 min at 12.00 h, an intersurge period. PRL increased in a dose-dependent manner and from this, the largest dose was used in subsequent experiments to ensure maximal opioid receptor stimulation. The next experiment defined the temporal sensitivity of the neuroendocrine system regulating PRL surges to exogenous β-End. Day 8 pregnant rats showed dramatic PRL responses to β-End when given at midnight (presurge) or 12.00 h (intersurge), but greatly attenuated responses at 02.00 h (early surge) and 04.00 h (late surge). Animals treated at 06.00 h (postsurge) showed recovered responsiveness to β-End. To determine what may account for the significantly lower PRL increases to β-End during the surge, day 8 pregnant rats received 100 ng/µl/min β-End i.c.v. for 15 min at 10.00 h, and then again at 12.00 h. All animals showed PRL increases greater than 1,140 ng/ml at 10.00 h, but the subsequent response to β-End at 12.00 h was reduced by 70%. In another experiment, β-End was infused at midnight and the animals were monitored for a subsequent endogenous nocturnal PRL surge. Although all animals showed a rapid increase in PRL following β-End treatment, 5 of 8 animals did not have a nocturnal PRL surge. This suggests that the initial β-End may downregulate its receptors, and therefore account for the much lower PRL response to β-End during the surge. To determine whether an insufficient amount of pituitary PRL may account for the small response to β-End during the surge, hemipituitary PRL concentration was measured. Pituitary PRL concentration was found to be lower at 04.00 h, when the incremental increase in plasma PRL to β-End was smallest, compared to the concentration at midnight, when the response was highest. However, at 02.00 h, pituitary PRL levels were similar to those at midnight, yet the PRL response to β-End differed greatly at these 2 times. Based on these results, lower pituitary PRL concentration during the nocturnal surge may only partially account for the attenuated PRL response to β-End. Downregulation of β-end receptors or less dopamine available for inhibition by β-End in the tuberoinfundibular dopamine neurons also are likely explanations.

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“…Diurnal variations in gonadotrophin release are clearly of importance in the attainment of reproductive competence (MacKinnon et al, 1978;Ojeda et al, 1986). Jacobson & Wilkinson (1986) have suggested that circadian variations in brain neurotransmitter binding sites (receptors; see also Wirz-Justice, 1987), and in particular hypothalamic opioid receptors, may entrain prepubertal hormone secretion. Since melatonin is now thought to be a timekeeping hormone (Karsch, 1986;Reiter, 1987), we wished to know whether the anti-pubertal effects of melatonin (Rivest et al, 1986;Lang, 1986) might be expressed as a disruption of hypothalamic opioid receptor binding rhythms.…”

Section: Introductionmentioning

confidence: 99%

Lack of effect of melatonin on sexual maturation in female rats

Badawi¹,

Wilkinson²

1988

Reproduction

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Daily subcutaneous injections of 100 \ g=m\ g melatonin given to prepubertal female rats housed in 14L:10D or 12L:12D failed to delay puberty as evidenced by the age at which vaginal opening occurred; neither the Sprague\p=n-\Dawley nor the Wistar strain rats were responsive to melatonin treatment. Reproductive organ weights (ovaries and uteri) at vaginal opening were unaffected by such treatment. Administration of melatonin through the drinking water in doses of 100, 500 or 1000 \g=m\g/day did not alter the timing of puberty or the reproductive organ weights in rats of the Sprague\p=n-\Dawley or Long\p=n-\Evans strains (housed in 12L:12D). Our experimental methods are identical to a previous report and we have no explanation for our failure to reproduce the earlier results.

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Association of Diurnal Variations in Hypothalamic but Not Cortical Opiate ([<sup>3</sup>H]-Naloxone)-Binding Sites with the Ability of Naloxone to Induce LH Release in the Prepubertal Female Rat

Cited by 17 publications

References 19 publications

Circadian and Estral Changes in the Hypothalamic Prostaglandin E₂ Content and [³H]Prostaglandin E₂ Binding in Female Rats

Circadian and Estral Changes in the Hypothalamic Prostaglandin E₂ Content and [³H]Prostaglandin E₂ Binding in Female Rats

Time-Dependent Changes in β-Endorphin-Stimulated Prolactin Release during Pregnancy

Lack of effect of melatonin on sexual maturation in female rats

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Association of Diurnal Variations in Hypothalamic but Not Cortical Opiate ([<sup>3</sup>H]-Naloxone)-Binding Sites with the Ability of Naloxone to Induce LH Release in the Prepubertal Female Rat

Cited by 17 publications

References 19 publications

Circadian and Estral Changes in the Hypothalamic Prostaglandin E2 Content and [3H]Prostaglandin E2 Binding in Female Rats

Circadian and Estral Changes in the Hypothalamic Prostaglandin E2 Content and [3H]Prostaglandin E2 Binding in Female Rats

Time-Dependent Changes in β-Endorphin-Stimulated Prolactin Release during Pregnancy

Lack of effect of melatonin on sexual maturation in female rats

Contact Info

Product

Resources

About

Circadian and Estral Changes in the Hypothalamic Prostaglandin E₂ Content and [³H]Prostaglandin E₂ Binding in Female Rats

Circadian and Estral Changes in the Hypothalamic Prostaglandin E₂ Content and [³H]Prostaglandin E₂ Binding in Female Rats