The alpha-7 nicotinic acetylcholine receptor is involved in a direct inhibitory effect of nicotine on GnRH release: In vitro studies

Messi, Elio; Pimpinelli, Federica; Andrè, Valentina; Rigobello, Chiara; Gotti, Cecilia; Maggi, Roberto

doi:10.1016/j.mce.2017.07.025

Cited by 9 publications

(9 citation statements)

References 71 publications

(80 reference statements)

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“…Although the precise mechanisms were not identified, these studies indicate that central mAChRs are involved in the GnRH/LH surge and subsequently ovulation. Work from rat hypothalamic cultures ( 14 ) and the mouse-derived GT1-7 GnRH cell line ( 15 – 17 ) showed that the nicotinic system can modulate the release of GnRH. Both ACh and nicotine stimulate GnRH release while muscarine inhibits it.…”

Section: Introductionmentioning

confidence: 99%

Acetylcholine regulation of GnRH neuronal activity: A circuit in the medial septum

Shostak

Constantin²,

Flannery³

et al. 2023

Front. Endocrinol.

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In vertebrates, gonadotropin-releasing hormone (GnRH)-secreting neurons control fertility by regulating gonadotrophs in the anterior pituitary. While it is known that acetylcholine (ACh) influences GnRH secretion, whether the effect is direct or indirect, and the specific ACh receptor (AChR) subtype(s) involved remain unclear. Here, we determined 1) whether ACh can modulate GnRH cellular activity and 2) a source of ACh afferents contacting GnRH neurons. Calcium imaging was used to assay GnRH neuronal activity. With GABAergic and glutamatergic transmission blocked, subtype-specific AChR agonists and antagonists were applied to identify direct regulation of GnRH neurons. ACh and nicotine caused a rise in calcium that declined gradually back to baseline after 5-6 min. This response was mimicked by an alpha3-specific agonist. In contrast, muscarine inhibited GnRH calcium oscillations, and blocking M2 and M4 together prevented this inhibition. Labeling for choline acetyltransferase (ChAT) and GnRH revealed ChAT fibers contacting GnRH neurons, primarily in the medial septum (MS), and in greater number in females than males. ChAT positive cells in the MS are known to express p75NGFRs. Labeling for p75NGFR, ChAT and GnRH indicated that ChAT fibers contacting GnRH cells originate from cholinergic cells within these same rostral areas. Together, these results indicate that cholinergic cells in septal areas can directly regulate GnRH neurons.

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Section: Introductionmentioning

confidence: 99%

Acetylcholine regulation of GnRH neuronal activity: A circuit in the medial septum

Shostak

Constantin²,

Flannery³

et al. 2023

Front. Endocrinol.

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“…5A). Essa risulta essere una capacità intrinseca dei neuroni GnRH ed è osservabile anche in cellule isolate [32,33].…”

Section: L'armoniosa Secrezione Pulsatile Del Gnrhunclassified

“…Ad esempio diversi nostri studi hanno potuto evidenziare il ruolo che i peptidi oppioidi endogeni (mediatori del dolore e di altre funzioni) [35][36][37] piuttosto che la nicotina [33,38] svolgono nella fine regolazione della secrezione del GnRH.…”

Section: Fig 5 A) Schema Dell'interazione Dei Neuroni Gnrh Con I Vasi Portali Ipofisarici E Della Secrezione Del Decapeptide Sono Indicatunclassified

Regolazione Della Fertilitã€: Arte E Neuroscienze

Maggi

2020

INCONTRI

Self Cite

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The term ‘fertility’ (from Latin language getting abundant harvests) leads back to several fields of the sciences; however, when it is linked to the physiology of reproduction it became, along with nutrition, as a fundamental behavior for the living species. The ‘mystery’ of human reproduction has been an attractive issue and extensively represented in figurative arts (paintings, sculptures, ect.) throughout the centuries and different cultures, being itself an ‘art’. Many scientists have been so fascinated by the art to have modified their personal and scientific lives. Art and sciences, in particular the neurosciences, share their origin during human history, being both the expression of human abilities to formulate an abstract thought to understand and describe the complexity of the world around us. For instance, paintings as the Cabanel’s Birth of Venus as well as the Primavera by Botticelli summarize several aspects of the sexual desire and reproduction; however, the neurosciences provide a more complex and artistic picture of the control of fertility. From the first descriptions, by Geoffrey Harris and Luciano Martini, of the control of the hormonal cascade governing reproductive functions by the hypothalamus, an important region of our brain, it came to the identification of the GnRH, the master regulator of hormonal reproductive axis. GnRH is produced by specific hypothalamic neurons and it is released in the blood vessels directed toward the pituitary gland in a pulsatile manner, finely tuned for rhythm and intensity, to regulate the secretion of pituitary gonadotropins LH and FSH. Released gonadotropin will exert trophic and regulatory effects on gonadal functions and on the production of sex hormones (testosterone and estrogens). A number of neuroendocrine signals control the development and the activity of GnRH neurons and whose functional alterations are responsible of several reproductive system diseases. According to the data so far available, it is fair to say that the development of such complex mechanisms, under the brain control, endowed with the extraordinary ability to create new individuals could be a real artwork.

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“…ACh exerts stimulatory and inhibitory effects on GnRH secretion in immortalized GnRH neurons, which express α7 nicotinic ACh receptors (AChRs) and M1, M2, and M4 muscarinic AChRs (111–113). Activation of α7 nicotinic ACh AChRs, which are non-selective cation channels, transiently increases basal GnRH secretion from immortalized GnRH neurons via depolarization followed by Ca 2+ influx through voltage-gated Ca 2+ channels (111, 112).…”

Section: Modulation Of Gnrh Neuron Activity and Secretion By Non-peptmentioning

confidence: 99%

“…Activation of α7 nicotinic ACh AChRs, which are non-selective cation channels, transiently increases basal GnRH secretion from immortalized GnRH neurons via depolarization followed by Ca 2+ influx through voltage-gated Ca 2+ channels (111, 112). It also inhibits prostaglandin E2 (PGE2)- and high K + -induced GnRH secretion (113), possibly due to Ca 2+ -dependent Ca 2+ channel inactivation. Activation of M1 muscarinic AChRs, which couple to G q , with micromolar concentrations of ACh, increases basal GnRH secretion from immortalized GnRH neurons via IP 3 -mediated Ca 2+ mobilization (111, 114), whereas activation of M2 and M4 muscarinic AChRs, which couple to G i , with nanomolar concentrations of ACh, inhibits basal GnRH secretion from immortalized GnRH neurons (111, 112).…”

Section: Modulation Of Gnrh Neuron Activity and Secretion By Non-peptmentioning

confidence: 99%

Modulation of Gonadotropin-Releasing Hormone Neuron Activity and Secretion in Mice by Non-peptide Neurotransmitters, Gasotransmitters, and Gliotransmitters

Spergel

2019

Front. Endocrinol.

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Gonadotropin-releasing hormone (GnRH) neuron activity and GnRH secretion are essential for fertility in mammals. Here, I review findings from mouse studies on the direct modulation of GnRH neuron activity and GnRH secretion by non-peptide neurotransmitters (GABA, glutamate, dopamine, serotonin, norepinephrine, epinephrine, histamine, ATP, adenosine, and acetylcholine), gasotransmitters (nitric oxide and carbon monoxide), and gliotransmitters (prostaglandin E2 and possibly GABA, glutamate, and ATP). These neurotransmitters, gasotransmitters, and gliotransmitters have been shown to directly modulate activity and/or GnRH secretion in GnRH neurons in vivo or ex vivo (brain slices), from postnatal through adult mice, or in embryonic or immortalized mouse GnRH neurons. However, except for GABA, nitric oxide, and prostaglandin E2, which appear to be essential for normal GnRH neuron activity, GnRH secretion, and fertility in males and/or females, the biological significance of their direct modulation of GnRH neuron activity and/or GnRH secretion in the central regulation of reproduction remains largely unknown and requires further exploration.

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The alpha-7 nicotinic acetylcholine receptor is involved in a direct inhibitory effect of nicotine on GnRH release: In vitro studies

Cited by 9 publications

References 71 publications

Acetylcholine regulation of GnRH neuronal activity: A circuit in the medial septum

Acetylcholine regulation of GnRH neuronal activity: A circuit in the medial septum

Regolazione Della Fertilitã€: Arte E Neuroscienze

Modulation of Gonadotropin-Releasing Hormone Neuron Activity and Secretion in Mice by Non-peptide Neurotransmitters, Gasotransmitters, and Gliotransmitters

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