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2 - The biology of puberty: new developments in sex differences

Published online by Cambridge University Press:  22 September 2009

By
Patricia Y. Fechner
Edited by
Chris Hayward
Patricia Y. Fechner
Affiliation:
Assistant Professor, Department of Pediatrics, Stanford University
Chris Hayward
Affiliation:
Stanford University, California
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Summary

At first glance puberty appears to be a discreet, isolated event that marks the transition from childhood to adulthood. In reality, though, it is part of a continuum of events that were initiated at conception. The hypothalamic gonadotropin releasing hormone (GnRH) pulse generator is initially active in fetal life and early infancy, but then suppressed during childhood; although at the onset of puberty it is reactivated. The etiology of this inhibition of the GnRH pulse generator is not known. It has been hypothesized that the onset of puberty is controlled by the brain “gonadostat,” which is a model used to describe the regulation of the hypothalamic GnRH pulse generator. Initially, in fetal life the gonadostat is insensitive to the negative feedback of gonadal sex steroids, testosterone in males and estrogen in females. But by the third trimester, the gonadostat has undergone some maturation and becomes sensitive to the high levels of estrogen and progesterone, and LH (luteinizing hormone) and FSH (follicle stimulating hormone) become suppressed. Through infancy and early childhood this sensitivity increases and the GnRH pulse generator is suppressed by the low levels of sex steroids. This feedback system is approximately ten times more sensitive to sex steroids than is the adult feedback mechanism (Styne and Grumbach, 1991). Then just prior to the onset of puberty, the sensitivity of the gonadostat to the negative feedback of gonadal sex steroids decreases, which releases the hypothalamic–pituitary axis from inhibition.

Type
Chapter
Information
Gender Differences at Puberty , pp. 17 - 28
Publisher: Cambridge University Press
Print publication year: 2003

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References

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