Neurokinin B signalling in human puberty

J Neuroendocrinol. 2010 Jul;22(7):765-70. doi: 10.1111/j.1365-2826.2010.02013.x. Epub 2010 Apr 29.

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.

Publication types

  • Review

MeSH terms

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

Substances

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