Control of Puberty in Non-Human Primates

Plant, Tony M.

doi:10.1007/978-1-59745-499-5_2

Cited by 4 publications

(3 citation statements)

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“…However, the identity of the gonadal hormone‐independent factor(s) is currently unknown, as is the specific age in development when this nongonadal suppression dissipates. Similar to male mice, in primates, there is gonadal hormone‐independent regulation of the developing reproductive axis, and puberty onset in primates appears to include removal of inhibitory input onto reproductive circuits, independent of changes in gonadal hormones (99, 100). However, the precise nongonadal inhibitory factor(s) involved remains unclear.…”

Section: Sex Differences In Arc Kiss1 Neurones Are Species‐specific Amentioning

confidence: 99%

Gonadal and Nongonadal Regulation of Sex Differences in Hypothalamic Kiss1 Neurones

Kauffman

2010

J Neuroendocrinology

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In vertebrates, physiology and behaviour, including aspects relating to reproduction and puberty, often vary between animals of the opposite sex. The neuroendocrine reproductive axis is governed by various hormonal and neural pathways that converge upon forebrain gonadotrophin-releasing hormone (GnRH) neurones (1). GnRH neurones direct the activation of the rest of the reproductive axis by stimulating the pituitary to synthesise and secrete gonadotrophins [luteinising hormone (LH) and follicle-stimulating hormone (FSH)], which regulate the gonads. GnRH neurones themselves do not appear to be sexually dimorphic, indicating that sex differences in the control of the reproductive axis likely reflect key sex differences in the afferent neural circuits and factors that regulate the GnRH system. However, many of the sexually-dimorphic factors that influence reproductive status have remained poorly defined. The newly-discovered kisspeptin system has recently been implicated as an important regulator of GnRH neurones, both in development and adulthood, and sex differences in the kisspeptin system may relate to sex differences in reproductive function. Here, the recent evidence that supports an important role of kisspeptin signalling in the control of the reproductive axis is reviewed, as well as how this relates to sexual differentiation of reproductive physiology. The roles of kisspeptin signalling in puberty and adulthood have already been extensively reviewed (2-4) and the focus herein is primarily on the latest findings connecting sexual differentiation and the kisspeptin system, specifically in rodent animal models. Journal of NeuroendocrinologyCorrespondence to: A. S. Kauffman, Department of Reproductive Medicine, Center for Chronobiology, University of California, San Diego, 9500 Gilman Drive, #0674 La Jolla, CA 92093, USA (e-mail: akauffman@ucsd.edu).The brains of males and females differ anatomically and physiologically, including sex differences in neurone size or number, synapse morphology and specific patterns of gene expression. Brain sex differences may underlie critical sex differences in physiology or behaviour, including several aspects of reproduction, such as the timing of sexual maturation (earlier in females than males) and the ability to generate a preovulatory gonadotrophin surge (in females only). The reproductive axis is controlled by afferent pathways that converge upon forebrain gonadotrophin-releasing hormone (GnRH) neurones, but GnRH neurones are not sexually dimorphic. Although most reproductive sex differences probably reflect sex differences in the upstream circuits and factors that regulate GnRH secretion, the key sexually-dimorphic factors that influence reproductive status have remained poorly defined. The recently-identified neuropeptide kisspeptin, encoded by the Kiss1 gene, is an important regulator of GnRH secretion, and Kiss1 neurones in rodents are sexually dimorphic in specific hypothalamic populations, including the anteroventral periventricular nucleus-periventricular nucleus ...

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Section: Sex Differences In Arc Kiss1 Neurones Are Species‐specific Amentioning

confidence: 99%

Gonadal and Nongonadal Regulation of Sex Differences in Hypothalamic Kiss1 Neurones

Kauffman

2010

J Neuroendocrinology

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“…The gonadotrophin‐releasing hormone (GnRH) neurones are the final output cells of the circuitry that governs fertility and, as such, activation of the GnRH neurones is critical for the initiation of puberty (1, 2). Many signalling molecules have been shown to play a role in the activation of GnRH neurones at puberty, including amino acid transmitters and neuropeptides.…”

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confidence: 99%

Gonadal Steroid Induction of Kisspeptin Peptide Expression in the Rostral Periventricular Area of the Third Ventricle During Postnatal Development in the Male Mouse

Clarkson

Shamas

Mallinson

et al. 2012

J Neuroendocrinology

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Kisspeptin and its G-protein coupled receptor Gpr54 are essential for the pubertal activation of gonadotrophin-releasing hormone (GnRH) neurones, with Gpr54 mutation or deletion resulting in failed puberty and infertility in humans and mice. The number of kisspeptin-immunoreactive neurones in the rostral periventricular area of the third ventricle (RP3V) increases during pubertal development in concert with the appearance of kisspeptin appositions with GnRH neurones in the mouse rostral preoptic area. We recently demonstrated that the pubertal increase in RP3V kisspeptin neuronal number in females is dependent upon circulating oestradiol levels. The present experiments investigated the potential role of gonadal steroids in the induction of kisspeptin expression in the RP3V during pubertal development in the male mouse. Using immunocytochemistry (ICC), we show that gonadectomy of male pups at postnatal day (P) 20 resulted in a 60-70% reduction in the number of kisspeptin immunoreactive (IR) neurones within the RP3V of P45 mice (P<0.05) compared to sham-treated littermates. We established a profile of circulating testosterone levels during postnatal development in male mice and found that circulating testosterone was low throughout early postnatal development and increased from P35-40 to reach adult levels. Treatment of P20-gonadectomised male mice with 17β-oestradiol or testosterone from P38-45 restored kisspeptin-IR neurone number in the RP3V to intact control levels (P>0.05). Using double-label ICC, we demonstrate that the majority of RP3V kisspeptin neurones express androgen receptors and oestrogen receptor α, indicating that RP3V kisspeptin neurones in the male mouse are equipped to respond to both androgen and oestrogen signals. These results indicate that, as in females, gonadal steroids are essential for the increase in kisspeptin immunoreactive cell number that occurs in the RP3V during pubertal development in the male mouse.

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“…Factors governing the neuroendocrine switch'' for the pulse generator, which is on 'in early infancy, then turns off during childhood, and switches back 'on' again at puberty have not been found. The list of factors which modulate the activity of the hypothalamo-Pituiary -Gonadal (HPG) Axes includes both inhibitory and and a reduction in inhibitory influences [1], the glial component is mainly facilitator and secreted both by growth factors and small molecules that directly or indirectly stimulate GnRH secretion [4]. The excitatory transsynaptic regulation of GnRH secretion is given by at least 3 different neuronal subsets: kisspeptin neurons acting via GPR54 receptors [5], glutamatergic neurons acting mostly via AMPA receptors [6,7] but also by NMDA receptors [7,8] and GABA acting via inotropic GABAA receptors [8].…”

Section: Initiation Of Puberty (Central Control Mechanism)mentioning

confidence: 99%

A Review on Update on Diagnosis and Therapeutic Management of Precocious Puberty’’ - A long with A Case Report

Kaur¹

2017

OAJG

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Precocious Puberty (PP) is the attainment of secondary sex characters before the age of 8 in girls and 9 yrs in boys. It can be divided into Central PP(CPP)/True PP or Gonadotropin dependent PP and Gonadotropon independent PP(GIPP) or Pseudo PP. CPP is characterized by the premature activation of the hypothalamo-Pituitary-Gonadal Axis. Onset of secondary sex characteristics before age 8, which further progresses with increased growth velocity and bone age acceleration which ultimately ends in impaired adult height. Mutation studies have shown occasional mutations in KISS1. KISS1R, Makorin ring finger protein 3(MKRN3) genes as some of the genetic modifications. Treatment with Gonadotropin releasing hormone agonists remain the treatment of choice which helps in ultimate attainment of normal height till actual age of puberty. With further introduction of a yearly GnRH subcutaneous implant histerelin administration has become more convenient than the tedious monthly GnRH a in the form of leuprolide depot or decapeptyl depot. This review sums up the various causes of CPP and GIPP with an update of its management, differential diagnosis and a case report to highlight an example.

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Control of Puberty in Non-Human Primates

Cited by 4 publications

References 76 publications

Gonadal and Nongonadal Regulation of Sex Differences in Hypothalamic Kiss1 Neurones

Gonadal and Nongonadal Regulation of Sex Differences in Hypothalamic Kiss1 Neurones

Gonadal Steroid Induction of Kisspeptin Peptide Expression in the Rostral Periventricular Area of the Third Ventricle During Postnatal Development in the Male Mouse

A Review on Update on Diagnosis and Therapeutic Management of Precocious Puberty’’ - A long with A Case Report

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