Α Melanocyte Stimulating Hormone Induces Gonadotropin Release

Reid, Robert L.; Ling, Nicholas; Yen, S. S. C.

doi:10.1210/jcem-52-1-159

Cited by 19 publications

(6 citation statements)

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“…As it is known that the ARC‐POMC neurons abundantly co‐express leptin receptors (Cheung et al 1997 a ; Finn et al 1998), and the α‐MSH‐containing axon terminals make direct synaptic contacts with GnRH neurons (Leranth et al 1988; Thind & Goldsmith, 1988; Chen et al 1989), the temporal relationship between α‐MSH and GnRH release during leptin infusion may suggest an intermediary role of α‐MSH in linking leptin and the activation of GnRH neurons. This view seems to be in keeping with several previous studies in vivo and in vitro conducted in both rats (Alde & Celis, 1980; Durando et al 1989; Caballero & Celis, 1993) and humans (Reid et al 1981; Limone et al 1997) that were in favour of α‐MSH as a stimulator to the GnRH‐LH system, although a few conflicting reports also exist (Khorram et al 1984; Scimonelli & Celis, 1990). In addition, it is also possible that the leptin‐induced release of α‐MSH, an anorectic peptide, is associated with ingestive behaviour.…”

Section: Discussionsupporting

confidence: 88%

Leptin directly acts within the hypothalamus to stimulate gonadotropin‐releasing hormone secretion in vivo in rats

Watanobe

2002

The Journal of Physiology

113

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It is still not known whether leptin, an adipocyte‐derived hormone, acts directly within the hypothalamus to stimulate the gonadotropin‐releasing hormone (GnRH)‐luteinizing hormone (LH) system. In order to address this question, the present study examined the effects of direct intrahypothalamic perfusions with leptin on the in vivo release of GnRH in ovarian steroid‐primed ovariectomized rats utilizing the push‐pull perfusion technique. Both α‐melanocyte‐stimulating hormone (α‐MSH) and neuropeptide Y were also measured in the hypothalamic perfusates. In normally fed animals, the leptin infusion was without effect on the release of these three hypothalamic peptides and also without effect on plasma LH and prolactin (PRL), whether leptin was infused into the medial preoptic area (where the majority of GnRH neuronal cell bodies exist) or the median eminence‐arcuate nucleus complex (where axon terminals of GnRH neurons are located). In contrast, in 3‐day fasted rats leptin was effective in stimulating the secretion of GnRH, α‐MSH, and LH, regardless of the site of perfusion. These three hormones were increased in a temporal order of α‐MSH, GnRH and LH. Irrespective of the site of perfusion, leptin was without effect on the release of neuropeptide Y. Only when leptin was infused into the median eminence‐arcuate nucleus complex was PRL secretion also stimulated, although its onset was 1 h behind that of LH. The leptin‐induced elevations of GnRH, α‐MSH, LH and PRL were all dose‐dependently stimulated by subnormal (1.0 ng ml−1) and normal (3.0 ng ml−1) concentrations of leptin, but at higher concentrations (10 ng ml−1) it did not produce additional effects. Leptin infusion into the anterior hypothalamic area, a control site equidistant from both the medial preoptic area and the median eminence‐arcuate nucleus complex, did not produce a significant change in any of the hormones in either the fed or fasted rats. These results demonstrate for the first time that leptin can act at both the cell bodies and axon terminals of GnRH neurons to stimulate the release of the neurohormone in vivo, and they also suggest that α‐MSH may play a significant intermediary role in linking leptin and GnRH secretion.

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Section: Discussionsupporting

confidence: 88%

Leptin directly acts within the hypothalamus to stimulate gonadotropin‐releasing hormone secretion in vivo in rats

Watanobe

2002

The Journal of Physiology

113

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“…Importantly, kisspeptin actions in the arcuate nucleus are essential to this pulse generation (Li et al, 2009). Activation of central melanocortin receptors stimulates GnRH pulse generator activity (Matsuyama et al, 2005) and gonadotropin secretion in humans (Reid et al, 1981) and rats (Watanobe et al, 1999). Thus, in addition to direct excitation on GnRH neurons, kisspeptin may regulate GnRH neuronal activity by exciting POMC neurons of the arcuate nucleus.…”

Section: Discussionmentioning

confidence: 99%

Kisspeptin Directly Excites Anorexigenic Proopiomelanocortin Neurons but Inhibits Orexigenic Neuropeptide Y Cells by an Indirect Synaptic Mechanism

Pol²

2010

J. Neurosci.

207

186

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The neuropeptide kisspeptin is necessary for reproduction, fertility, and puberty. Here, we show strong kisspeptin innervation of hypothalamic anorexigenic proopiomelanocortin (POMC) cells, coupled with a robust direct excitatory response by POMC neurons (n Ͼ 200) to kisspeptin, mediated by mechanisms based on activation of a sodium/calcium exchanger and possibly opening of nonselective cation channels. The excitatory actions of kisspeptin on POMC cells were corroborated with quantitative PCR data showing kisspeptin receptor GPR54 expression in the arcuate nucleus, and the attenuation of excitation by the selective kisspeptin receptor antagonist, peptide 234. In contrast, kisspeptin inhibits orexigenic neuropeptide Y (NPY) neurons through an indirect mechanism based on enhancing GABAmediated inhibitory synaptic tone. In striking contrast, gonadotropin-inhibiting hormone (GnIH and RFRP-3) and NPY, also found in axons abutting POMC cells, inhibit POMC cells and attenuate the kisspeptin excitation by a mechanism based on opening potassium channels. Together, these data suggest that the two central peptides that regulate reproduction, kisspeptin and GnIH, exert a strong direct action on POMC neurons. POMC cells may hypothetically serve as a conditional relay station downstream of kisspeptin and GnIH to signal the availability of energy resources relevant to reproduction.

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“…Another interesting result of our experiment is the lack of effect of morphine in animals in which it was administered concomitantly with inflammatory pain; in these animals, the stimulatory effect on steroid hormones and receptors was completely lost. To explain this effect, we must consider that the inflammatory pain reaction induces an increase in cytokines, such as IL-6, and stress related-hormones known to interfere with steroidogenesis at different levels, including the adrenal and ovary [35][36][37]. These cytokines, as well as stressrelated hormones, are capable of reducing LH levels [38,39], thereby counterbalancing the stimulatory effects of morphine when given alone.…”

Section: Discussionmentioning

confidence: 99%

Gonadal ERα/β, AR and TRPV1 gene expression: Modulation by pain and morphine treatment in male and female rats

Vodo

Arcelli

Fiorenzani

et al. 2013

Physiology & Behavior

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Α Melanocyte Stimulating Hormone Induces Gonadotropin Release

Abstract: The present study demonstrates that synthetic alpha-MSH given as a 2.5 mg intravenous bolus induces an unequivocal rise in LH and FSH in male subjects but not in female subjects during the low estrogen phase of the cycle.

Cited by 19 publications

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Leptin directly acts within the hypothalamus to stimulate gonadotropin‐releasing hormone secretion in vivo in rats

Leptin directly acts within the hypothalamus to stimulate gonadotropin‐releasing hormone secretion in vivo in rats

Kisspeptin Directly Excites Anorexigenic Proopiomelanocortin Neurons but Inhibits Orexigenic Neuropeptide Y Cells by an Indirect Synaptic Mechanism

Gonadal ERα/β, AR and TRPV1 gene expression: Modulation by pain and morphine treatment in male and female rats

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