Opposite-sex housing reactivates the declining GnRH system in aged transgenic male mice with FGF signaling deficiency

Rochester, Johanna R.; Chung, Wilson C.J.; Hayes, Tyrone B.; Tsai, Pei‐San

doi:10.1152/ajpendo.00289.2012

Cited by 9 publications

(10 citation statements)

References 63 publications

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“…GnRH neurons respond to endogenous Kp concomitantly with their morphological remodeling 15 , however, the functional link between these two events has not been previously explored. To date, complex GnRH dendritic morphology was reported in only one mouse model exhibiting delayed puberty and fertility defects 23 , yet the functional relevance of the immature GnRH morphologies was not explored 23 . In our study, we found an increase of complex/immature GnRH dendritic morphology in the OVLT in nes::cre;Dmxl2 wt/loxp mice, associated with a decrease of unipolar morphology, and no changes in the bipolar GnRH dendritic morphology.…”

Section: Discussionmentioning

confidence: 99%

Rabconnectin-3α is required for the morphological maturation of GnRH neurons and kisspeptin responsiveness

Tata

Harbulot

Peineau

et al. 2017

Sci Rep

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A few hundred hypothalamic neurons form a complex network that controls reproduction in mammals by secreting gonadotropin-releasing hormone (GnRH). Timely postnatal changes in GnRH secretion are essential for pubertal onset. During the juvenile period, GnRH neurons undergo morphological remodeling, concomitantly achieving an increased responsiveness to kisspeptin, the main secretagogue of GnRH. However, the link between GnRH neuron activity and their morphology remains unknown. Here, we show that brain expression levels of Dmxl2, which encodes the vesicular protein rabconnectin-3α, determine the capacity of GnRH neurons to be activated by kisspeptin and estradiol. We also demonstrate that Dmxl2 expression levels control the pruning of GnRH dendrites, highlighting an unexpected role for a vesicular protein in the maturation of GnRH neuronal network. This effect is mediated by rabconnectin-3α in neurons or glial cells afferent to GnRH neurons. The widespread expression of Dmxl2 in several brain areas raises the intriguing hypothesis that rabconnectin-3α could be involved in the maturation of other neuronal populations.

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Section: Discussionmentioning

confidence: 99%

Rabconnectin-3α is required for the morphological maturation of GnRH neurons and kisspeptin responsiveness

Tata

Harbulot

Peineau

et al. 2017

Sci Rep

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“…GnRH neurons are essential for epididymo-testicular descent and the onset and maintenance of sexual reproduction. Proper specification of GnRH cell fate, both prenatally and postnatally, relies on FGFs [ 11 ], and the developing GnRH system is highly sensitive to reduced levels of FGF signaling [ 12 ]. FGF-mediated signaling is involved in mitogenesis, proliferation, differentiation, cellular migration, angiogenesis, and tissue injury repair [ 13 ].…”

Section: Epididymo-testicular Descentmentioning

confidence: 99%

On the descent of the epididymo-testicular unit, cryptorchidism, and prevention of infertility

Hadžiselimović

2017

Basic Clin. Androl.

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This comprehensive review provides in-depth coverage of progress made in understanding the molecular mechanisms underlying cryptorchidism, a frequent pathology first described in about 1786 by John Hunter. The first part focuses on the physiology, embryology, and histology of epididymo-testicular descent. In the last 20 years epididymo-testicular descent has become the victim of schematic drawings with an unjustified rejection of valid histological data. This part also includes discussion on the roles of gonadotropin-releasing hormone, fibroblast growth factors, Müllerian inhibiting substance, androgens, inhibin B, and insulin-like 3 in epididymo-testicular descent. The second part addresses the etiology and histology of cryptorchidism as well as the importance of mini-puberty for normal fertility development. A critical view is presented on current clinical guidelines that recommend early orchidopexy alone as the best possible treatment. Finally, by combining classical physiological information and the output of cutting-edge genomics data into a complete picture the importance of hormonal treatment in preventing cryptorchidism-induced infertility is underscored.

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“…This is relevant for when considering reversible CHH as relatively few GnRH neurons are necessary for inducing pulsatile LH secretion (56). Further, murine studies suggest that the GnRH system is highly plastic as environmental stimuli such as sexual interactions can rescue GnRH function in some instances (57). Further, epigenetic influences seem also to play a critical role in the onset of puberty (58), and thus potentially in the reversal process.…”

Section: Etiology Of Chh Reversalmentioning

confidence: 99%

MANAGEMENT OF ENDOCRINE DISEASE: Reversible hypogonadotropic hypogonadism

Dwyer

Raivio

Pitteloud

2016

European Journal of Endocrinology

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Congenital hypogonadotropic hypogonadism (CHH) is characterized by lack of puberty and infertility. Traditionally, it has been considered a life-long condition yet cases of reversibility have been described wherein patients spontaneously recover function of the reproductive axis following treatment. Reversibility occurs in both male and female CHH cases and appears to be more common (~10-15%) than previously thought. These reversal patients span a range of GnRH deficiency from mild to severe and many reversal patients harbor mutations in genes underlying CHH. However, to date there are no clear factors for predicting reversible CHH. Importantly, recovery of reproductive axis function may not be permanent. Thus, CHH is not always life-long and the incidence of reversal warrants periodic treatment withdrawal with close monitoring and follow-up. Reversible CHH highlights the importance of environmental (epigenetic) factors such as sex steroid treatment on the reproductive axis in modifying the phenotype. This review provides an overview and an update on what is known about this phenomenon.

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Opposite-sex housing reactivates the declining GnRH system in aged transgenic male mice with FGF signaling deficiency

Abstract: Rochester JR, Chung WC, Hayes TB, Tsai PS. Opposite-sex housing reactivates the declining GnRH system in aged transgenic male mice with FGF signaling deficiency.

Cited by 9 publications

References 63 publications

Rabconnectin-3α is required for the morphological maturation of GnRH neurons and kisspeptin responsiveness

Rabconnectin-3α is required for the morphological maturation of GnRH neurons and kisspeptin responsiveness

On the descent of the epididymo-testicular unit, cryptorchidism, and prevention of infertility

MANAGEMENT OF ENDOCRINE DISEASE: Reversible hypogonadotropic hypogonadism

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