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.
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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)
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Chemical References |
- Receptors, Neurokinin-3
- Tachykinins
- Gonadotropin-Releasing Hormone
- Dynorphins
- Neurokinin B
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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)
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