Noradrenaline and Prostaglandin E&lt;sub&gt;2&lt;/sub&gt; Stimulate LH-RH Release from Rat Median Eminence through Distinct 1-Alpha-Adrenergic and PGE&lt;sub&gt;2&lt;/sub&gt; Receptors

Héaulme, Michel; Dray, F.

doi:10.1159/000124012

Cited by 56 publications

(6 citation statements)

References 13 publications

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“…That the interaction of NPY and LHRH may be of physiological significance is also suggested by our observation that the potency of NPY in stimulating basal LHRH release (submicromolar to mi cromolar range) is comparable to other known excitatory neurochemicals, such as NE [16, 28. 31] or prostaglandin E: [16,30,31] for which the evidence of physiological involve ment in LH secretion has been presented [17,21], It remains to be determined how the ovarian steroid mi lieu alters the responses of LHRH neurons to stimuli from another peptidergic system, such as seen in the case of NPY. The facilitatory response due to steroids may involve changes in NPY reception or in signal transduction subseq uent to binding to receptors, as well as effects on the availa ble pool of LHRH as a result of augmented synthesis and processing of LH RH [8,9, 17, 23-25, 33, 35].…”

Section: Discussionmentioning

confidence: 99%

“…It is possible that NPY may mo dulate LHRH release either directly, or indirectly, by chan ging the catecholamine input to the LHRH neurons in the hypothalamus. Therefore, the objectives of the present studies were to test whether NPY, like NE [7,16,28,31], can stimulate in vitro release of LH RH from the nerve terminals of the median eminence and whether the direction of the LHRH response, as implied by in vivo studies [18], is de pendent upon ovarian hormone pretreatment. Addi tionally, these studies evaluated the effects of NPY on the in vitro release of NE and dopamine (DA) simultaneously with LHRH.…”

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confidence: 99%

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Neuropeptide Y Stimulates the Release of Luteinizing Hormone-Releasing Hormone from Medial Basal Hypothalamus in vitro: Modulation by Ovarian Hormones

1987

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These studies investigated the effects of neuropeptide Y (NPY) on in vitro release of luteinizing hormone-releasing hormone (LHRH) from the medial basal hypothalmus (MBH) and tested whether ovarian steroids modulate the LHRH response to NPY. Ovariectomized rats were implanted with 20-mm-long Silastic capsules containing a low concentration of estradiol (E₂) (150 µg/ml oil), a high concentration of E₂(250 µg/ml oil), or sesame oil vehicle. Additional animals received high-dose E₂ capsules plus an injection of progesterone (15 mg) concomitantly. Two days later, individual MBH fragments were incubated in medium alone for a 30-min period to obtain the basal rate of LHRH release, followed by a second 30-min period in medium containing NPY or saline. Exposure to NPY (10^–6M) increased the release of LHRH from MBH of ovarian hormone-treated, but not from hormonally untreated rats. The LHRH response was most pronounced from the MBH of rats treated with either high-dose E₂ or E₂ plus progesterone. The increase in LHRHrelease was also elicited by 10^–7M, but not by 10^–8M NPY concentrations, using MBH from E₂ plus progesterone-treated rats. In addition, NPY markedly potentiated the KCl-evoked release of LHRH from MBH of ovariectomized, hormonally untreated or low-dose E₂-treated rats, under conditions when there was little or no effect of NPY on the basal LHRH release. Further, the release of LHRH stimulated by NPY was not accompanied by increase in the release of norepinephrine or of dopamine. These results strongly suggest that the NPY stimulation of LH secretion after intracerebral administration in steroid-primed rats occurs, in part, as a result of increased release of LHRH. NPY may act at the level of the LHRH neurosecretory terminals in the median eminence as well as at additional sites containing LHRH perikarya.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Neuropeptide Y Stimulates the Release of Luteinizing Hormone-Releasing Hormone from Medial Basal Hypothalamus in vitro: Modulation by Ovarian Hormones

1987

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“…A detailed pharmacological analysis, which was carried out on a culture of the interstitial Cells of the testes of mice, showed that the production of androgens is activated only after the stimulation of the ~2-adrenoreceptors, which according to our data, do not participate in sexual activation. Consequently, it can be held that in our experiments the adrenoblockers exerted an effect at the level of the hypothalamus, since ~l-adrenoreceptors which participate in the regulation of the secretion of luliberin have been found in the median eminence of rats [13]. In addition, it was shown that the administration of prazosin does not have an influence on the increase in the T level in the blood of rats induced by chorionic gonadotropin [9].…”

Section: Resultsmentioning

confidence: 46%

Role of adrenoreceptors in the activation of the hypothalamo-hypophyseo-testicular complex of mice elicited by the presence of the female

Науменко

Amstislavskaya

Осадчук

1990

Neurosci Behav Physiol

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The initial components of the sexual behavior of the male is its motivation, determined by the presence of a receptive female even without direct contact with her. The stimulation, dependent upon the genotype, of the hypothaiamo-hypophyseo-testicular complex takes place in male mice under such conditions [2]. The results we have previously obtained [I] have provided a basis for the conclusion that adrenergic mechanisms participate in the regulatio n of the endocrine function of the testes during sexual motivation, that the activating influences are realized through the a-adrenoreceptors, and the inhibiting influences are realized through the ~-adrenoreceptors. However it is known at the present time that both the a-, and the ~-adrenoreceptors are represented by functionally different subtypes: el, a2 [4,5] and 91, ~2 [4,14]. Which of the subtypes of the adrenoreceptors participate in the regulation of the hypothalamo-hypophyseo-testicular complex during sexual activation elicited by the presence of a receptive female remain unknown. At the same time this problem is important for the understanding of the mechanisms of the regulation of the endocrine function of the testes, as well as for the prospects for the possibile pharmacological correction of pathologically expressed sexual motivation. The elucidation of the role of the individual subtypes of the adrenoreceptors in sexual activation elicited only in the presence of a receptive female was in fact the goal of the present study. MATERIALS AND METHODSThe experiment was carried out in male mice of two hybrid lines, CBA/Lac and A/He at the age of 2.5-3.0 months. The animals were born and raised in the Institute's vivarium in natural illumination. Food and water were obtained without limitations.Five days before the experiment the mice were placed in separate cages divided by a mesh barrier into two halves, and were trained to the hand for ten minutes daily. After five days a female of the BALB/c line, in estrus elicited by the successive administration of estradiol and progesterone, was presented to each male for 40 min in the free half of the cage. Adrenobiockers which exerted an effect primarily on one of the four subtypes of adrenoreceptors were used in the experiments: prazosin, which blocks ~i-[6], yohimbine, which blocks a 2-[12], metoprolol, which blocks 81-[I0], and optimol, which blocks the 82-adrenoreceptors [Ii], were used in the experiments. The prazosin and the yohimbine were dissolved in 0.04 ml of glacial acid immediately before administration, and were diluted to the necessary concentration with equal volumes of twice-distilled water and physiological solution. The metoprolol and the optimol were dissolved in physiological solution. All the preparations were administered subcutaneously in a volume of 0.i ml of the appropriate solvent, which was also used for the administration to the control animals, 30 min prior to the presentation of the female. Those doses of the adrenoblockers which did not exert a substantial influence on the initial level of ...

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“…On the other hand, the release of immunoreactive GnRH in vitro from the rat hypothalamus can be stimulated by potassium [22][23][24], ATP and magnesium [25], prostaglandin E? [22,26,27], dopamine [24,28], and norepi nephrine [26,28,29], Whether the regula tion of T4 on the release of GnRH reflects a direct effect on hypothalamic GnRH neu rons or an indirect effect through catechol amine turnover or influx of ions is unknown. Our data do not rule out the possibility that other hypothalamic agents can influence the release of LH as well.…”

Section: Discussionmentioning

confidence: 99%

Effects of Thyroidectomy and Thyroxine Replacement on the Release of Luteinizing Hormone and Gonadotropin-Releasing Hormone in vitro

Wang¹,

Pu²,

Chiang³

et al. 1987

Horm Res

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The effects of thyroidectomy and thyroxine (T4) replacement on the release of luteinizing hormone (LH) and gonadotropin-releasing hormone (GnRH) in ovariectomized (Ovx) rats were studied. Immediately after ovariectomy, rats were thyroidectomized (Tx) or sham-Tx. The Ovx-Tx rats were injected subcutaneously with either saline or T4 (2 µg/100 g body weight) daily for 30 days before sacrifice. Sham-Tx rats were treated with saline only. Twenty hours after the last injection, the blood sample was obtained by decapitation. The excised anterior pituitary gland (AP) was bisected and incubated in vitro with or without 0.1 0.5, 2.5, and 50 ng GnRH at 37 °C for 4 h. The mediobasal hypothalamus (MBH) was bisected and incubated with or without the AP of Ovx donor rat in vitro. Concentrations of LH and GnRH in the medium and that of LH in the serum were measured by radioimmunoassay. LH in the serum of Tx rats was higher than that in the serum of sham-Tx and Tx-T4 rats. Thyroidectomy resulted in an increase of LH release by Ovx rat AP, stimulated with or without 0.1 and 50 ng GnRH, as well as in an increase of immunoreactive GnRH release from MBH of Ovx rats in vitro. After a 4-hour incubation with donor APs, the LH in the medium containing MBH obtained from Tx rats was significantly higher than that obtained from sham-Tx and Tx-T4 rats. LH concentrations, in both sera and media, as well as GnRH concentration in the media of euthyroid and T4-replaced Tx groups were nonsignificantly different. These results suggest that T4 is inhibitory to the basal and GnRH-stimulated LH release as well as to the release of GnRH in the absence of ovarian hormones.

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Noradrenaline and Prostaglandin E<sub>2</sub> Stimulate LH-RH Release from Rat Median Eminence through Distinct 1-Alpha-Adrenergic and PGE<sub>2</sub> Receptors

Cited by 56 publications

References 13 publications

Neuropeptide Y Stimulates the Release of Luteinizing Hormone-Releasing Hormone from Medial Basal Hypothalamus in vitro: Modulation by Ovarian Hormones

Neuropeptide Y Stimulates the Release of Luteinizing Hormone-Releasing Hormone from Medial Basal Hypothalamus in vitro: Modulation by Ovarian Hormones

Role of adrenoreceptors in the activation of the hypothalamo-hypophyseo-testicular complex of mice elicited by the presence of the female

Effects of Thyroidectomy and Thyroxine Replacement on the Release of Luteinizing Hormone and Gonadotropin-Releasing Hormone in vitro

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