2020Current Opinion in Endocrine and Metabolic ResearchOpen access

Neuroendocrine mechanisms of puberty in non–human primates

Ei Terasawa, James P. Garcia

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Abstract

An increase in pulsatile release of gonadotropin-releasing hormone (GnRH) initiates puberty in mammalian species. While mutations in KISS1 and TAC3 and their receptors, KISS1R and NK3R, respectively, result in the absence or abnormal timing of puberty, the neurocircuitry and precise role of kisspeptin and neurokinin B (NKB) in regulation of the GnRH neurosecretory system in primate puberty remain elusive. This article discusses how kisspeptin and NKB signaling contributes to the pubertal increase in GnRH release in non–human primates and how remodeling of the NKB and kisspeptin signaling circuitry controlling GnRH neurons takes place during the progress of puberty. Importantly, the pubertal remodeling of kisspeptin and NKB signaling ensures efficient functions of the GnRH neurosecretory system that regulates sex-specific reproduction in primates.

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An increase in pulsatile release of gonadotropin-releasing hormone (GnRH) initiates puberty in mammalian species. While mutations in KISS1 and TAC3 and their receptors, KISS1R and NK3R, respectively, result in the absence or abnormal timing of puberty, the neurocircuitry and precise role of kisspeptin and neurokinin B (NKB) in regulation of the GnRH neurosecretory system in primate puberty remain elusive. This article discusses how kisspeptin and NKB signaling contributes to the pubertal increase in GnRH release in non–human primates and how remodeling of the NKB and kisspeptin signaling circuitry controlling GnRH neurons takes place during the progress of puberty. Importantly, the pubertal remodeling of kisspeptin and NKB signaling ensures efficient functions of the GnRH neurosecretory system that regulates sex-specific reproduction in primates.

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Available abstract

An increase in pulsatile release of gonadotropin-releasing hormone (GnRH) initiates puberty in mammalian species. While mutations in KISS1 and TAC3 and their receptors, KISS1R and NK3R, respectively, result in the absence or abnormal timing of puberty, the neurocircuitry and precise role of kisspeptin and neurokinin B (NKB) in regulation of the GnRH neurosecretory system in primate puberty remain elusive. This article discusses how kisspeptin and NKB signaling contributes to the pubertal increase in GnRH release in non–human primates and how remodeling of the NKB and kisspeptin signaling circuitry controlling GnRH neurons takes place during the progress of puberty. Importantly, the pubertal remodeling of kisspeptin and NKB signaling ensures efficient functions of the GnRH neurosecretory system that regulates sex-specific reproduction in primates.

Key concepts: Kisspeptin, Neurokinin B, Internal medicine, Endocrinology, Gonadotropin-releasing hormone, Biology, Hypothalamic–pituitary–gonadal axis, Receptor

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