Gonadotropin-Releasing Hormone Release from the Rat Hypothalamus: Dependence on Membrane Depolarization and Calcium Influx*

Bigdeli, Homayoon; Snyder, Peter J.

doi:10.1210/endo-103-1-281

Cited by 56 publications

(26 citation statements)

References 19 publications

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“…We have recently described a hypothalamic incubation system that offers the possibility of investigating the factors that regulate GnRH secretion (6). GnRH release into the incubation medium in this system is linear for 1 h; stimulated by membrane-depolarizing concentrations of potassium and ouabain; and is inhibited by omitting calcium from the incubation medium or by blocking calcium uptake with verapamil.…”

Section: Discussionmentioning

confidence: 99%

“…GnRH release in the hypothalamic incubation system employed here has been shown to depend on membrane depolarization and calcium uptake (6) Incubation. Hypothalami were removed and incubated as described (6). The hypothalami were placed, one per tube, in incubation medium at 37°C.…”

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confidence: 91%

“…GnRH was assayed by a modification of the method of Nett et al (8), with anti-GnRH generously provided by them. The modification was as described (6), except that the oxidizing agent used for the preparation of [1251]iodoGnRH was chloramine T (5 ,ug), rather than lactoperoxidase, because the stability of ['251]iodo-GnRH prepared with lactoperoxidase varied with the batch of lactoperoxidase. Binding of [1251]iodo-GnRH to anti-GnRH was optimum at pH 7.0-7.2; assay reagents were therefore titrated to pH 7.2 (6).…”

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confidence: 99%

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Administration of Gonadal Steroids to the Castrated Male Rat Prevents a Decrease in the Release of Gonadotropin-Releasing Hormone from the Incubated Hypothalamus

Rudenstein¹,

Bigdeli²,

McDonald³

et al. 1979

J. Clin. Invest.

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A B S T R A C T The influence of testosterone on gonadotropin-releasing hormone (GnRH) secretion was assessed indirectly by altering the serum testosterone concentration of male rats and measuring GnRH release from their incubated hypothalami 1 wk later.GnRH release from hypothalami ofcastrated rats was 13.4±+1.2 (SE) pg/h, compared to 35.3±3.8 pg/h from hypothalami of intact rats (P < 0.001). GnRH release from the hypothalami of castrated rats treated with testosterone propionate, 100 or 500 ,ug daily, was 25.0±3.4 pg/h and 27.9±3.6 pg/h, which is significantly greater (P < 0.05 and P < 0.01, respectively) than that from hypothalami of castrated rats treated only with sesame oil. A similar decrease in GnRH release from hypothalami of hypophysectomized rats and prevention of this decrease by treating the hypophysectomized rats with testosterone propionate is evidence that the observed effects of testosterone are not mediated via luteinizing hormone and(or) follicle-stinriulating hormone secretion. Treatment of castrated rats with either dihydrotestosterone propionate or estradiol benzoate also prevented the decrease in GnRH release from the hypothalami of castrated rats.We conclude that testosterone, dihydrotestosterone, and estradiol all prevent the decrease in GnRH release from hypothalami of castrated rats treated with these steroids. The possibility exists that these steroids may also maintain GnRH secretion in vivo.

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Section: Discussionmentioning

confidence: 99%

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confidence: 91%

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confidence: 99%

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Administration of Gonadal Steroids to the Castrated Male Rat Prevents a Decrease in the Release of Gonadotropin-Releasing Hormone from the Incubated Hypothalamus

Rudenstein¹,

Bigdeli²,

McDonald³

et al. 1979

J. Clin. Invest.

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“…Glutamergic and noradrenergic terminals stimulate the NOergic neuron to release NO by action on their receptors to increase intracellular free calcium in the NOergic neurons, and the calcium combines with calmodulin that activates neural NO synthase (NOS), causing synthesis and release of NO from the neurons. Previous experiments have shown that LH-RH is released from medial basal hypothalamic explants by membrane depolarization by high potassium concentrations [K ϩ ] (24,25), by the specific stimulant Nmethyl-D-aspartate (NMDA) (26)(27)(28)(29)(30)(31)(32), and by a releaser of NO, nitroprusside (NP) (18,26,30,33), whereas inhibition of NO synthesis with the competitive inhibitor of the enzyme N Gmonomethyl-L-arginine (NMMA) blocked NMDA-induced stimulation of LH-RH release, indicating the crucial role of NO in the response.…”

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confidence: 99%

Ascorbic acid acts as an inhibitory transmitter in the hypothalamus to inhibit stimulated luteinizing hormone-releasing hormone release by scavenging nitric oxide

Karanth

Yu²,

Walczewska³

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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Because ascorbic acid (AA) is concentrated in synaptic vesicles containing glutamic acid, we hypothesized that AA might act as a neurotransmitter. Because AA is an antioxidant, it might therefore inhibit nitric oxidergic (NOergic) activation of luteinizing hormonereleasing hormone (LH-RH) release from medial basal hypothalamic explants by chemically reducing NO. Cell membrane depolarization induced by increased potassium concentration [K ؉ ] increased medium concentrations of both AA and LH-RH. An inhibitor of NO synthase (NOS), N G -monomethyl-L-arginine (NMMA), prevented the increase in medium concentrations of AA and LH-RH induced by high [K ؉ ], suggesting that NO mediates release of both AA and LH-RH. Calcium-free medium blocked not only the increase in AA in the medium but also the release of LH-RH. Sodium nitroprusside, which releases NO, stimulated LH-RH release and decreased the concentration of AA in the incubation medium, presumably because the NO released oxidized AA to dehydro-AA. AA (10 ؊5 to 10 ؊3 M) had no effect on basal LH-RH release but completely blocked high [K ؉ ]-and nitroprusside-induced LH-RH release. N-Methyl-D-aspartic acid (NMDA), which mimics the action of the excitatory amino acid neurotransmitter glutamic acid, releases LH-RH by releasing NO. AA (10 ؊5 to 10 ؊3 M) inhibited the LH-RH-releasing action of NMDA. AA may be an inhibitory neurotransmitter that blocks NOergic stimulation of LH-RH release by chemically reducing the NO released by the NOergic neurons.is present in high concentrations in the hypothalamus (1-3) but its role in the modulation of hypothalamic hormone release is obscure. The brain accumulates AA from the blood and maintains a relatively high concentration (1.1-1.7 mM), independent of AA ingestion (4-7). Neuronal intracellular AA concentrations are 10 times greater than extracellular AA concentration (6, 7). Neuronal activity was shown to increase extracellular AA in vitro (6,(8)(9)(10)(11)(12) and in vivo as determined by voltametry (13). AA is further concentrated in isolated nerve terminals (14). Synaptic vesicles concentrate AA by active transport (15). AA is present in high concentrations in synaptic vesicles of glutamergic neurons (13) and in adrenal medullary catecholamine secretory granules (16,17).The presence of high concentrations of AA in synaptic vesicles and the evidence that it could be released into the extracellular space by neuronal activity suggested to us that AA might be a neurotransmitter. Since high concentrations of AA are already known to be present in the hypothalamus, we hypothesized that AA might control luteinizing hormone-releasing hormone (LH-RH) release, possibly by its antioxidant properties. LH-RH release is controlled by release of nitric oxide (NO) from NOergic interneurons that release the soluble gas in juxtaposition to the LH-RH terminals (18,19). In the terminals, NO activates guanylyl cyclase, leading to an increase in cyclic guanosine monophosphate (cGMP), cyclooxygenase, resulting in increased concentrations of prostagla...

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“…Prostaglandin E2 (PGE2) stimulates the release of luteinizing hormone-releasing hormone (LH-RH) from hypothalamic tissue incubated under in vitro conditions (1)(2)(3)(4)(5), and this stimulation has a partial requirement for the influx of extracellular calcium (1,6). Several lines of evidence strongly suggest that, as in other secretory cells, calcium influx coupled to an increase in the intracellular levels of cAMP serve as a major intracellular pathway mediating PGE2 action on the LH-RH neuron or on other neurons, the secretory products of which stimulate LH-RH release.…”

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Copper amplification of prostaglandin E2 stimulation of the release of luteinizing hormone-releasing hormone is a postreceptor event.

Barnea¹,

Cho²

1987

Proc. Natl. Acad. Sci. U.S.A.

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We have shown that copper amplifies prostaglandin E2 (PGE2) stimulation of luteinizing hormonereleasing hormone (LH-RH) from explants of the median eminence area (MEA) and that this process is calciumdependent. Since a Ca-cAMP pathway has been implicated in PGE2 action on the LH-RH neuron, in this study we wished to ascertain if copper exerts its effect on the PGE2 receptor or on a postreceptor component involved in PGE2 To test these three possibilities, we evaluated the effects of copper on the stimulation of LH-RH release by PGE2 (reaction 1), forskolin (reaction 2), and 8-bromoadenosine 3',5'-cyclic monophosphate (8-bromo-cAMP) (reaction 3), using an in vitro system of median eminence area (MEA) explants. For comparison, we assessed the effect of copper on LH-RH release stimulated by depolarizing concentration of K+, a Ca2+-dependent release process that does not involve an increase in cAMP levels. Our results strongly support the conclusion that copper modulates the functional state of a postreceptor component that is integral to the Ca-cAMP pathway stimulated by PGE2. MATERIALS AND METHODSIn Vitro Incubation. Long Evans male rats (200-250 g) were used. The MEA was dissected (15) 580The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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Gonadotropin-Releasing Hormone Release from the Rat Hypothalamus: Dependence on Membrane Depolarization and Calcium Influx*

Cited by 56 publications

References 19 publications

Administration of Gonadal Steroids to the Castrated Male Rat Prevents a Decrease in the Release of Gonadotropin-Releasing Hormone from the Incubated Hypothalamus

Administration of Gonadal Steroids to the Castrated Male Rat Prevents a Decrease in the Release of Gonadotropin-Releasing Hormone from the Incubated Hypothalamus

Ascorbic acid acts as an inhibitory transmitter in the hypothalamus to inhibit stimulated luteinizing hormone-releasing hormone release by scavenging nitric oxide

Copper amplification of prostaglandin E2 stimulation of the release of luteinizing hormone-releasing hormone is a postreceptor event.

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