Novel Biology of Tachykinins in Gonadotropin-Releasing Hormone Secretion

2019 ◽  
Vol 37 (03) ◽  
pp. 109-118 ◽  
Author(s):  
Silvia Leon ◽  
Víctor M. Navarro
Keyword(s):  
Hormone Secretion ◽  
Gonadotropin Releasing Hormone ◽  
Optimal Timing ◽  
Releasing Hormone ◽  
Open Questions ◽  
Reproductive Axis ◽  
Gnrh Release ◽  
Timing Of Puberty ◽  
Puberty Onset ◽  
Luteinizing Hormone Surge

AbstractThe tachykinin family of peptides, composed of the neurokinins A and B (NKA, NKB) and substance P are involved in the central control of gonadotropin-releasing hormone (GnRH) release through a variety of neuronal circuitries that mediate the activation of Kiss1 neurons and the synchronization of their activity within the arcuate nucleus. The major outcome of this role is the precise regulation of the pulsatile pattern of GnRH release. In addition, tachykinins are involved in the maturation of the reproductive axis by determining the optimal timing of puberty onset, as well as in the timing of the preovulatory luteinizing hormone surge in females. Therefore, the action of tachykinins in reproduction appears to extend to all the critical aspects required for the successful attainment and maintenance of fertility. In this review, we summarize the latest advances in our understanding of the biology of tachykinins in the control of GnRH release, addressing the existing controversies, open questions, and future perspectives.

Activins and their receptors in female reproduction

2000 ◽  
Vol 78 (3) ◽  
pp. 261-279 ◽  
Author(s):  
Chun Peng ◽  
Spencer T Mukai
Keyword(s):  
Transforming Growth Factor ◽  
Hormone Secretion ◽  
Transforming Growth Factor Β ◽  
Gonadotropin Releasing Hormone ◽  
Receptor Expression ◽  
Type I ◽  
Female Reproduction ◽  
Hormone Production ◽  
Releasing Hormone ◽  
Reproductive Axis

Activins are growth and differentiation factors belonging to the transforming growth factor-β superfamily. They are dimeric proteins consisting of two inhibin β subunits. The structure of activins is highly conserved during vertebrate evolution. Activins signal through type I and type II receptor proteins, both of which are serine/threonine kinases. Subsequently, downstream signals such as Smad proteins are phosphorylated. Activins and their receptors are present in many tissues of mammals and lower vertebrates where they function as autocrine and (or) paracrine regulators of a variety of physiological processes, including reproduction. In the hypothalamus, activins are thought to stimulate the release of gonadotropin-releasing hormone. In the pituitary, activins increase follicle-stimulating hormone secretion and up-regulate gonadotropin-releasing hormone receptor expression. In the ovaries of vertebrates, activins are expressed predominantly in the follicular layer of the oocyte where they regulate processes such as folliculogenesis, steroid hormone production, and oocyte maturation. During pregnancy, activin-A is also involved in the regulation of placental functions. This review provides a brief overview of activins and their receptors, including their structures, expression, and functions in the female reproductive axis as well as in the placenta. Special effort is made to compare activins and their receptors in different vertebrates. Key words: activins, activin receptors, reproductive axis, placenta.

N-methyl-D,L-aspartate (NMDA) stimulates gonadotropin secretion in the ovine fetus through gonadotropin-releasing hormone (GnRH) release

1988 ◽  
Vol 117 (4_Suppl) ◽  
pp. S93-S94
Author(s):  
M. BETTENDORF ◽  
F. DE ZEGHER ◽  
N. ALBERS ◽  
S. L. KAPLAN ◽  
M. M. GRUMBACH
Keyword(s):  
Gonadotropin Releasing Hormone ◽  
Gonadotropin Secretion ◽  
Releasing Hormone ◽  
Gnrh Release ◽  
Ovine Fetus

scholarly journals Distinct Mechanisms Involving Diverse Histone Deacetylases Repress Expression of the Two Gonadotropin β-Subunit Genes in Immature Gonadotropes, and Their Actions Are Overcome by Gonadotropin-Releasing Hormone

2007 ◽  
Vol 27 (11) ◽  
pp. 4105-4120 ◽  
Author(s):  
Stefan Lim ◽  
Min Luo ◽  
Mingshi Koh ◽  
Meng Yang ◽  
Mohammed Nizam bin Abdul Kadir ◽  
...  
Keyword(s):  
Histone Deacetylases ◽  
Reproductive Function ◽  
Gonadotropin Releasing Hormone ◽  
Β Subunit ◽  
Releasing Hormone ◽  
Calcium Calmodulin Dependent ◽  
Gnrh Release ◽  
Dependent Protein ◽  
Reproductive Cycles ◽  
Class Iia Hdacs

ABSTRACT The gonadotropins luteinizing hormone (LH) and follicle-stimulating hormone (FSH) are produced in the embryonic pituitary in response to delivery of the hypothalamic gonadotropin releasing hormone (GnRH). GnRH has a pivotal role in reestablishing gonadotropin levels at puberty in primates, and for many species with extended reproductive cycles, these are reinitiated in response to central nervous system-induced GnRH release. Thus, a clear role is evident for GnRH in overcoming repression of these genes. Although the mechanisms through which GnRH actively stimulates LH and FSH β-subunit (FSHβ) gene transcription have been described in some detail, there is currently no information on how GnRH overcomes repression in order to terminate reproductively inactive stages. We show here that GnRH overcomes histone deacetylase (HDAC)-mediated repression of the gonadotropin β-subunit genes in immature gonadotropes. The repressive factors associated with each of these genes comprise distinct sets of HDACs and corepressors which allow for differentially regulated derepression of these two genes, produced in the same cell by the same regulatory hormone. We find that GnRH activation of calcium/calmodulin-dependent protein kinase I (CaMKI) plays a crucial role in the derepression of the FSHβ gene involving phosphorylation of several class IIa HDACs associated with both the FSHβ and Nur77 genes, and we propose a model for the mechanisms involved. In contrast, derepression of the LH β-subunit gene is not CaMK dependent. This demonstration of HDAC-mediated repression of these genes could explain the temporal shut-down of reproductive function at certain periods of the life cycle, which can easily be reversed by the actions of the hypothalamic regulatory hormone.

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