Normal Pubertal Physiology in Females

Boswell, Hillary B.

doi:10.1007/978-1-4939-0912-4_2

Cited by 7 publications

(12 citation statements)

References 72 publications

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“…In both sexes, circulating gonadal steroids (predominately estradiol and progesterone in girls and testosterone in boys, although both sexes experience rises in all three hormones at puberty) rise across puberty until reaching adult concentrations (Boswell, 2014; Rilling et al, 1996). In girls, the rise in circulating estradiol first manifests externally through the start of breast development (Divall and Radovick, 2008; Marshall and Tanner, 1969), which is followed 1–3 years later by first menses (menarche) (Anderson and Must, 2005; Hansen et al, 1975) and eventual ovulation and regular menstrual cyclicity within another 1–3 years (Boswell, 2014; Divall and Radovick, 2008; Legro et al, 2000). In boys, milestones are more difficult to observe; the first external indicator of puberty onset occurs with testosterone-induced increase in testicular volume along with a change in the color and texture of the scrotal skin (Marshall and Tanner, 1970; Sørensen et al, 2010).…”

Section: Comparing Pubertal Milestones In Humans and Rodent Modelsmentioning

confidence: 99%

Does puberty mark a transition in sensitive periods for plasticity in the associative neocortex?

et al. 2017

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Postnatal brain development is studded with sensitive periods during which experience dependent plasticity is enhanced. This enables rapid learning from environmental inputs and reorganization of cortical circuits that matches behavior with environmental contingencies. Significant headway has been achieved in characterizing and understanding sensitive period biology in primary sensory cortices, but relatively little is known about sensitive period biology in associative neocortex. One possible mediator is the onset of puberty, which marks the transition to adolescence, when animals shift their behavior toward gaining independence and exploring their social world. Puberty onset correlates with reduced behavioral plasticity in some domains and enhanced plasticity in others, and therefore may drive the transition from juvenile to adolescent brain function. Pubertal onset is also occurring earlier in developed nations, particularly in unserved populations, and earlier puberty is associated with vulnerability for substance use, depression and anxiety. In the present article we review the evidence that supports a causal role for puberty in developmental changes in the function and neurobiology of the associative neocortex. We also propose a model for how pubertal hormones may regulate sensitive period plasticity in associative neocortex. We conclude that the evidence suggests puberty onset may play a causal role in some aspects of associative neocortical development, but that further research that manipulates puberty and measures gonadal hormones is required. We argue that further work of this kind is urgently needed to determine how earlier puberty may negatively impact human health and learning potential.

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Section: Comparing Pubertal Milestones In Humans and Rodent Modelsmentioning

confidence: 99%

Does puberty mark a transition in sensitive periods for plasticity in the associative neocortex?

et al. 2017

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“…Si bien hay evidencias del vínculo entre KISS y el eje somatotrópico, hasta el momento no se ha establecido un mecanismo de relevancia fisiológica con respecto a la regulación de la secreción de GH por parte de KISS (47) . La generalidad de los autores proponen que las acciones positivas de GH en la pubertad y otras funciones reproductivas son efectuadas principalmente a través del IGF-I (48) ; no obstante algunos de sus efectos son ejercidos sin la intervención de dicho factor (49) . Debido a que en este trabajo no se encontraron efectos de KISS-10 en la secreción de GH, no se profundizará más en ese aspecto; sin embargo, debido a que en algunos trabajos efectuados en bovinos (4,6) la KISS-10 incrementó la liberación de GH, sería recomendable determinar las condiciones fisiológicas y de desarrollo en las que KISS evoca un aumento de GH de manera simultánea al de las gonadotropinas hipofisiarias, ya que potencialmente en esas situaciones la KISS exógena podría ser más efectiva en la inducción de la ovulación y el mejoramiento de otras funciones reproductivas.…”

Section: Discussionunclassified

Kisspeptin in prepuberal heifers: 2. Response of LH, FSH and GH to different doses of kisspeptin-10 and its association with circulating IGF-I and leptin

Godoy

Echeverría

Fernández

et al. 2018

Rev. Mex. Cienc. Pecu.

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En becerras prepúberes, la kisspeptina-10 (KISS-10) estimula la liberación de hormona luteinizante (LH) y hormona foliculoestimulante (FSH), pero su acción en la hormona del crecimiento (GH) es inconsistente. La hipótesis fue que en becerras prepúberes la magnitud de liberación de LH, FSH y GH en respuesta a KISS-10 es determinada por la dosis y las concentraciones endógenas de IGF-I y leptina. Se usaron 20 becerras prepúberes (100-232 kg de peso y 7-11 meses de edad), mismas que recibieron un bolo i.v. de 5 o 50 µg de KISS-10/kg de peso. Ambas dosis de KISS-10 indujeron un incremento de LH y FSH, más no de GH. La dosis de 50 µg de KISS-10 indujo un área bajo la curva de LH y una duración del incremento de FSH mayores (P<0.05) que la dosis de 5 µg. IGF-I se relacionó negativamente con el aumento de LH en respuesta a la dosis de 50 µg (P<0.05), pero no estuvo asociado con la respuesta de LH a la dosis de 5 µg de KISS-10. La magnitud del incremento de FSH y las concentraciones de GH posteriores a KISS-10 no fueron alteradas por las concentraciones de IGF-I (P>0.05). De la misma forma, las concentraciones de leptina no determinaron (P>0.05) la magnitud del incremento de LH y FSH ni las concentraciones de GH pos tratamiento. En conclusión, la GH no respondió a ninguna dosis, pero la FSH y la LH fueron sensibles al aumento de dosis de KISS-10. Además, la magnitud de respuesta de LH a KISS-10 fue determinada por las concentraciones endógenas de IGF-I, pero no de leptina.

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“…All models were adjusted for relevant developmental and biosocial covariates [14,18]; only significant predictors were maintained. Sample sizes differed between the models because we had an incomplete dataset for some variables.…”

Section: Methodsmentioning

confidence: 99%

Father's death does not affect growth and maturation but hinders reproduction: evidence from adolescent girls in post-war Estonia

Hõrak

Valge

2015

Biol. Lett.

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The popular concept of predictive-adaptive responses poses that girls growing up without a father present in the family mature and start reproduction earlier because the father's absence is a cue for environmental harshness and uncertainty that favours switching to a precocious life-history strategy. Most studies supporting this concept have been performed in situations where the father's absence is caused by divorce or abandonment. Using a dataset of Estonian adolescent girls who had lost their fathers over the period of World War II, we show that father's death did not affect the rate of pubertal maturation (assessed on the basis of development of breasts and axillary hair) or growth. Father's death did not affect the age of first birth but, contrary to predictions, reduced lifetime reproductive success. Our findings thus do not support the concept of predictive-adaptive responses and suggest that alternative explanations for covariation between fatherlessness and early maturation are required.

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Normal Pubertal Physiology in Females

Cited by 7 publications

References 72 publications

Does puberty mark a transition in sensitive periods for plasticity in the associative neocortex?

Does puberty mark a transition in sensitive periods for plasticity in the associative neocortex?

Kisspeptin in prepuberal heifers: 2. Response of LH, FSH and GH to different doses of kisspeptin-10 and its association with circulating IGF-I and leptin

Father's death does not affect growth and maturation but hinders reproduction: evidence from adolescent girls in post-war Estonia

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