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The neurobiology of primate puberty
1University of Pittsburgh School of Medicine, Department of Physiology, PA 15261.
Insights
In higher primates, a neural brake suppresses gonadotropin-releasing hormone (GnRH) release during development. Puberty onset involves the reactivation of this GnRH network, controlled by a central timing mechanism.
Area of Science:
- Reproductive endocrinology
- Neuroendocrinology
- Primate development
Background:
- Higher primates exhibit a prolonged prepubertal developmental phase.
- This phase is characterized by suppressed pulsatile hypothalamic gonadotropin-releasing hormone (GnRH) secretion.
- This suppression maintains the quiescence of the pituitary-gonadal axis in juveniles.
Purpose of the Study:
- To investigate the mechanism suppressing GnRH release in prepubertal higher primates.
- To understand the neurobiological basis of the prolonged juvenile developmental phase.
- To identify factors regulating the onset of puberty in primates.
Main Methods:
- Utilized the rhesus monkey as a model organism.
- Measured GnRH release indirectly via luteinizing hormone (LH) secretion from the in situ pituitary.
- Employed physiological, neuroanatomical, and neuropharmacological approaches to study the prepubertal GnRH regulation.
Main Results:
- Identified a prepubertal 'brake' on pulsatile GnRH release in rhesus monkeys.
- This brake appears to be a withdrawal of synchronized, frequency-facilitated afferent neural input to the GnRH network.
- The GnRH network itself shows properties similar to postpubertal animals.
Conclusions:
- The prepubertal hiatus in GnRH release is due to the loss of specific neural input.
- Puberty onset is linked to the reactivation of synchronous activity in the GnRH network.
- A central neural time- or growth-tracking device is proposed to time puberty onset.
Abstract:
In higher primates the protracted prepubertal phase of development is occasioned by a mechanism that suppresses pulsatile hypothalamic gonadotropin-releasing hormone (GnRH) secretion from late infancy until the onset of puberty and thereby guarantees, in the juvenile, the quiescence of the pituitary-gonadal axis. Studies from our laboratory have employed the rhesus monkey, a representative higher primate, as an experimental paradigm. GnRH release has been measured using luteinizing hormone secretion by the in situ pituitary as a bioassay for the hypothalamic hormone. The nature of the prepubertal brake on pulsatile GnRH release in the monkey has been probed using physiological, neuroanatomical and neuropharmacological approaches. Such studies have led to the view that the prepubertal hiatus in pulsatile GnRH release results from a withdrawal in late infancy of a synchronized frequency-facilitated afferent neural input to the GnRH network, which in all other respects appears to exhibit properties identical to those in the postpubertal animal. The mechanism timing the onset of puberty, i.e. that responsible for the reactivation of synchronous activity in the GnRH network, is posited to be under the control of a central neural time- or growth-tracking device.