Medial Preoptic Area Involvement in Norepinephrine-Induced Suppression of Pulsatile Luteinizing Hormone Release in Ovariectomized Rats

Leipheimer, Robert E.; Gallo, Robert V.

doi:10.1159/000124097

Cited by 37 publications

(16 citation statements)

References 17 publications

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“…There is, however, also evidence that a NE-receptive preoptic mechanism is inhibitory to LH pulsatility. Leipheimer and Gallo [17] infused contin uously minute, in our view physiologic, amounts of NE into the PO/AH which reduced LH pulse frequency. It is, therefore, possible that continuous exposure of Gn-RH neurons to NE is inhibitory, whereas intermittent, randomly occurring NE sig nals stimulate these neurons.…”

Section: Resultsmentioning

confidence: 67%

A Norepinephrine-Dependent Mechanism in the Preoptic/Anterior Hypothalamic Area but Not in the Mediobasal Hypothalamus Is Involved in the Regulation of the Gonadotropin-Releasing Hormone Pulse Generator in Ovariectomized Rats

Jarry

Leonhardt

Wuttke³

1990

Neuroendocrinology

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Pulsatile gonadotropin secretion from the pituitary is dependent upon the gonadotropin-releasing hormone (Gn-RH) pulse generator producing intermittent release of the neuropeptide into the portal vessels. Various neurotransmitters seem to be involved in the regulation of pulsatile Gn-RH release. The present study was an attempt to determine in vivo the temporal relation of preoptic/anterior hypothalamic area (PO/AH) norepinephrine (NE) release and pulsatile luteinizing hormone (LH) secretion in ovariectomized rats. To assess whether NE acts in the PO/AH to maintain pulsatile Gn-RH release, we applied locally an αi-receptor antagonist into this structure. Push-pull cannulae (PPC) were implanted into the PO/AH of ovariectomized rats. The contralateral, not PPC-implanted PO/AH was lesioned electrochemically. Another group of ovariectomized rats was implanted with a PPC into the mediobasal hypothalamus. Two experiments were performed: (1) To determine whether the PO/AH or the mediobasal hypothalamus is the site where NE exerts its stimulatory effect on LH secretion, we applied doxazosine, a new specific αi-receptor antagonist, locally into these structures by means of PPC. The effect of this adrenergic drug on the Gn-RH pulse generator was examined by measuring blood LH levels. (2) To study the temporal relation between in vivo release rates of NE and amine metabolites in the preoptic area and pulsatile pituitary LH secretion, preoptic perfusates and blood samples were collected at 5-min intervals. Brain perfusates were subjected to high-performance liquid chromatography-electrochemical analysis. In blood samples LH concentrations were determined. Local application of doxazosine into the PO/AH, but not into the mediobasal hypothalamus caused a reduction of average LH secretion and reduced markedly LH pulsatility. This is suggestive that preoptic NE is indispensable for proper function of the Gn-RH pulse generator and that NE exerts its stimulatory effect on LH release via αi-receptive mechanisms in the PO/AH. Preoptic perfusates contained readily detectable amounts of NE which is secreted in a pulsatile manner. Frequency analysis revealed that the number of NE pulses in the PO/AH is significantly higher than the number of LH pulses in the blood. Using two different statistical approaches, we failed to demonstrate a temporal correlation between preoptic NE release and pituitary LH secretion. Based on these data, we hypothesize that phasic activitity of Gn-RH neurons is achieved by NE which exerts a permissive function rather than a direct stimulatory effect of Gn-RH neurons. Our data do not support the assumption that, at least in the rat, each Gn-RH pulse is triggered by a NE pulse.

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Section: Resultsmentioning

confidence: 67%

A Norepinephrine-Dependent Mechanism in the Preoptic/Anterior Hypothalamic Area but Not in the Mediobasal Hypothalamus Is Involved in the Regulation of the Gonadotropin-Releasing Hormone Pulse Generator in Ovariectomized Rats

Jarry

Leonhardt

Wuttke³

1990

Neuroendocrinology

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“…Thus, in regularly cycling animals which have been exposed to endogenous ste roids [2] or in rats that have been treated with steroids |3, 4], intracerebroventricular administration of catecholamines stim ulates LH release. Whereas, in ovariectomized animals which have been deprived of ovarian steroids for varying lengths of time, infusion of norepinephrine into the medial preoptic area [5] or cerebral ventricles (3, 4], or electrical stimulation of the dorsal tegmental tract (6] inhibits LH release. Most evidence Received: December 15, 1988 Accepted after revision: April 10, 1989 suggests that the stimulatory effects of norepinephrine on LHRH are mediated by a 1-adrenergic receptors [7][8][9][10] and possibly « 2-adrenergic receptors (11-13), whereas the inhibi tory effects are mediated by [f-adrenergic receptors (14-18], These data have led many investigators to speculate that ste roids dictate whether norepinephrine stimulates or inhibits LH by altering the relative concentrations of at-and (1-adrenergic receptors either on LHRH neurons themselves or on intemeurons in the pathway from catecholamine cell bodies in the midand hind-brain to the LHRH neurons in the hypothalamus (14].…”

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confidence: 99%

Diurnal Rhythmicity of Beta-1- and Beta-2-Adrenergic Receptors in Ovariectomized, Ovariectomized Estradiol-Treated and Proestrous Rats

Weiland

Wise²

1989

Neuroendocrinology

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The effect of norepinephrine on LH is complex: the ovarian steroidal milieu appears to determine whether norepinephrine stimulates or inhibits LH secretion. It has been proposed that steroids allow norepinephrine to have opposite effects on LH by altering the relative concentrations of α₁-(stimulatory) and β-(inhibitory) adrenergic receptors in the hypothalamus. Thus, many investigators have argued that estradiol may permit norepinephrine to stimulate LH release by increasing the density of α₁- and decreasing the density of β-adrenergic receptors in one or more key hypothalamic regions. To test this hypothesis specifically, we measured the density of β₁- and β₂-adrenergic receptor densities in proestrous, ovariectomized, and ovariectomized estradiol-treated rats at various times of day to determine (1) whether the densities of β-receptors exhibit diurnal rhythmicity, (2) whether β-receptors decrease during the time of increased LH secretion and/or (3) how steroidal milieu influences the density and/or the rhythm of receptor densities. The densities of β₁- and β₂-receptors exhibit a diurnal rhythm in some brain areas. These rhythms are detectable only in proestrous and ovariectomized rats and only in selected brain regions. Estrogen treatment has opposing effects in different brain regions. It suppresses the rhythm of β₁-receptor concentrations in ovariectomized rats and also suppresses the average density of receptors in the suprachiasmatic nucleus and pineal gland. In contrast, estrogen increases the density of β₁-receptors in the medial preoptic nucleus. In summary, the results of this study demonstrate that the diurnal rhythm in β-receptors and the effect of estradiol correlate with previously reported changes in receptor-mediated functions. In addition, they reveal the complex interactions of time of day and steroidal milieu on the density of β₁- and β₂-receptors in various brain regions. Finally, the data strongly suggest that decreases in the densities of β-receptors cannot explain the timing of the proestrous or estradiol-induced LH surge or the ability of norepinephrine to inhibit LH release in ovariectomized rats or stimulate LH release in steroid-treated rats.

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“…Perhaps more importantly, grouping elevated the M HPG/NE ratio, which is one technique used to estimate NE activity, compared to controls and male-treated ani mals. Leipheimer and Gallo [35] have described an inhibi tory role for NE in the ovariectomized rat which acts in the POA to suppress LH pulse frequency. If NE plays a similar role in the POA of the mouse, then one way in which grou ping suppresses puberty may be by influencing LH pulse frequency.…”

Section: Discussionmentioning

confidence: 99%

Neuroendocrine Responses to Social Regulation of Puberty in the Female House Mouse

1992

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First estrus is advanced in female house mice exposed to an adult male and delayed in those housed in groups. Experiments were conducted to explore possible mechanisms by which the hypothalamus integrates these puberty-regulating social signals. Female mice weaned at 21 days of age were placed in groups of 8 (G8JF), a juvenile female with a juvenile male (JFJM) or juvenile female with an adult male (JFAM). All females were ovariectomized on day 28 and sacrificed on day 29. There was no significant difference between treatments in the postovariectomy rise in LH. Next, female mice were weaned, assigned to G8JF, JFJM or JFAM treatments and ovariectomized on day 22. Females were sacrificed on day 29, 3 h after injection with either 1.0 µg of estradiol, or vehicle. Estradiol significantly suppressed LH in all three treatments, with no differences between treatments. Two-way ANOVA (social treatment × estradiol treatment) revealed no differences or interactions in brain catecholamines as a result of estradiol injection. The G8JF treatment significantly increased norepinephrine, (NE), dopamine (DA) and its metabolite 3,4-dihydroxy-phenylacetic acid in the mediobasal hypothalamus (MBH), and the 3-methoxy-4-hydroxy-phenylglycol/NE ratio in the preoptic area (POA). In the final experiments, isolate prepubertal female mice were treated with either water or male urine (MU) on the oronasal groove. Eight days of MU treatment resulted in significant uterine growth, however there were no differences in serum LH, POA or MBH catecholamines or POA and median eminence LHRH. One hour after application of MU, serum LH was significantly elevated, however, there were no differences in accessory olfactory bulb catecholamines. These results suggest that the mechanism by which male and grouped female exposure alters first estrus may not involve changes in sensitivity to estradiol negative feedback. Grouping may delay first estrus through the negative effects of DA on the LHRH system in the MBH. We observed no differences that might help to explain how male exposure causes LH release.

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Medial Preoptic Area Involvement in Norepinephrine-Induced Suppression of Pulsatile Luteinizing Hormone Release in Ovariectomized Rats

Cited by 37 publications

References 17 publications

A Norepinephrine-Dependent Mechanism in the Preoptic/Anterior Hypothalamic Area but Not in the Mediobasal Hypothalamus Is Involved in the Regulation of the Gonadotropin-Releasing Hormone Pulse Generator in Ovariectomized Rats

A Norepinephrine-Dependent Mechanism in the Preoptic/Anterior Hypothalamic Area but Not in the Mediobasal Hypothalamus Is Involved in the Regulation of the Gonadotropin-Releasing Hormone Pulse Generator in Ovariectomized Rats

Diurnal Rhythmicity of Beta-1- and Beta-2-Adrenergic Receptors in Ovariectomized, Ovariectomized Estradiol-Treated and Proestrous Rats

Neuroendocrine Responses to Social Regulation of Puberty in the Female House Mouse

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