New genetic factors implicated in human GnRH-dependent precocious puberty: The role of kisspeptin system

Teles, Milena Gurgel; Silveira, Letícia Ferreira Gontijo; Tusset, Cíntia; Latrônico, Ana Claudia

doi:10.1016/j.mce.2011.05.019

Cited by 55 publications

(24 citation statements)

References 80 publications

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“…Moreover, pulsatile secretion of LH is restored in these patients by administration of kisspeptin-10 [54], suggesting that NKB operates upstream of kisspeptin in an autostimulatory fashion. Inactivating mutations in KiSS1R cause a similar hypogonadotropic hypogonadism phenotype in humans [10,109], and gain-of-function mutations in KiSS1 and KiSS1R result in GnRH-dependent precocious puberty [110,111]. Taken together, these data highlight the intimate synergistic relationship between the kisspeptin/GPR54 and NKB/NK3R signalling systems in the regulation of reproductive function.…”

Section: Revising the Modelmentioning

confidence: 96%

The Role of Neurokinin B Signalling in Reproductive Neuroendocrinology

2013

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The KNDy neuropeptides, kisspeptin, neurokinin B (NKB) and dynorphin A (Dyn), have been implicated in regulating pulsatile luteinising hormone (LH) secretion. Studies of the interactions between KNDy signalling systems, however, are currently few. Although the stimulatory effect of kisspeptin and the inhibitory effect of Dyn on the gonadotropin-releasing hormone pulse generator are widely accepted, the effects of NKB in rodents are variable and sometimes controversial. Literature describing increased LH secretion in response to NKB receptor agonism predominates and is in line with human physiology, as well as the pathophysiology of pubertal failure associated with disruption of NKB signalling. However, the robust suppression of the LH pulse, induced by the same treatment under hypoestrogenic conditions, may hold clues as to the mechanisms of reproductive inhibition under pathological conditions. This review discusses the recent evidence for this paradox and outlines a revised working model incorporating the mechanisms by which KNDy neuropeptides modulate the reproductive axis.

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Section: Revising the Modelmentioning

confidence: 96%

The Role of Neurokinin B Signalling in Reproductive Neuroendocrinology

2013

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“…Further knowledge can be gained through identification of gene defects underlying disorders where the normal timing of puberty is disrupted, such as in ICPP. Several genes, including KISS1, KISS1R, GNRHR, LIN28B, LIN28A, GABRA1, NPY1R, TAC3, and TACR3, have been proposed as candidate genes in ICPP based on genetic linkage and/or function of the gene product, but conclusive evidence for disease-causing mutations in these genes has not been found (2).…”

mentioning

confidence: 99%

A missense mutation in MKRN3 in a Danish girl with central precocious puberty and her brother with early puberty

et al. 2015

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“…Some neuroimaging studies suggest the existence of a series of activational effects in the amygdala and prefrontal cortex; in fact, both show higher sexual dimorphism during puberty and adolescence because of their dissimilar levels of gonadal hormones. Such effects would partially explain the differences in emotion and affection between both sexes (Van Wingen et al 2011). …”

Section: Sexual Dimorphism In the Adolescent Brainmentioning

confidence: 99%

Influence of Sex Steroid Hormones on the Adolescent Brain and Behavior: An Update

Vigil

Del

Carrera³

et al. 2016

Linacre Q

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This review explains the main effects exerted by sex steroids and other hormones on the adolescent brain. During the transition from puberty to adolescence, these hormones participate in the organizational phenomena that structurally shape some brain circuits. In adulthood, this will propitiate some specific behavior as responses to the hormones now activating those neural circuits. Adolescence is, then, a critical "organizational window" for the brain to develop adequately, since steroid hormones perform important functions at this stage. For this reason, the adolescent years are very important for future behaviors in human beings. Changes that occur or fail to occur during adolescence will determine behaviors for the rest of one's lifetime. Consequently, understanding the link between adolescent behavior and brain development as influenced by sex steroids and other hormones and compounds is very important in order to interpret various psycho-affective pathologies.Lay Summary: The effect of steroid hormones on the development of the adolescent brain, and therefore, on adolescent behavior, is noticeable. This review presents their main activational and organizational effects. During the transition from puberty to adolescence, organizational phenomena triggered by steroids structurally affect the remodeling of brain circuits. Later in adulthood, these changes will be reflected in behavioral responses to such hormones. Adolescence can then be seen as a fundamental "organizational window" during which sex steroids and other hormones and compounds play relevant roles. The understanding of the relationship between adolescent behavior and the way hormones influence brain development help understand some psychological disorders.

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New genetic factors implicated in human GnRH-dependent precocious puberty: The role of kisspeptin system

Cited by 55 publications

References 80 publications

The Role of Neurokinin B Signalling in Reproductive Neuroendocrinology

The Role of Neurokinin B Signalling in Reproductive Neuroendocrinology

A missense mutation in MKRN3 in a Danish girl with central precocious puberty and her brother with early puberty

Influence of Sex Steroid Hormones on the Adolescent Brain and Behavior: An Update

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