Neurokinin B signalling in human puberty.

Abstract

Recent identification of TAC3 or TACR3 (encoding neurokinin B and its receptor, NK3R, respectively) mutations as the causes of normosmic idiopathic hypogonadotrophic hypogonadism has provided compelling evidence for the involvement of neurokinin B (NKB) signalling in puberty. A surge of subsequent studies pointing towards an understanding of the exact mechanism through which NKB signalling exerts its effects in puberty led to a postulated sketch of the GnRH pulse generator, in which kisspeptin, NKB and dynorphin work in concert to elicit pulsatile gonadotrophin-releasing hormone release in the median eminence.

• Authors: A K Topaloglu, L D Kotan, B Yuksel
• Journal: Journal of neuroendocrinology (J Neuroendocrinol) Vol. 22 Issue 7 Pg. 765-70 (Jul 2010) ISSN: 1365-2826 [Electronic] United States
• PMID: 20456599 (Publication Type: Journal Article, Review)

Chemical References

• Receptors, Neurokinin-3
• Tachykinins
• Gonadotropin-Releasing Hormone
• Dynorphins
• Neurokinin B

Topics

• Animals
• Dynorphins (metabolism)
• Gonadotropin-Releasing Hormone (metabolism)
• Humans
• Median Eminence (metabolism)
• Mutation
• Neurokinin B (genetics, metabolism)
• Puberty (physiology)
• Receptors, Neurokinin-3 (genetics, metabolism)
• Signal Transduction (physiology)
• Tachykinins (genetics, metabolism)