Neurokinin B signalling in human puberty.
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.
Topaloglu
A K
AK
Faculty of Medicine, Department of Pediatric Endocrinology and Metabolism, Cukurova University, Balcali, Adana, Turkey. ktopaloglu@cu.edu.tr
Kotan
L D
LD
Yuksel
B
B
D000818:Animals; D004399:Dynorphins / Q000378:metabolism; D007987:Gonadotropin-Releasing Hormone / Q000378:metabolism; D006801:Humans; D008473:Median Eminence / Q000378:metabolism; D009154:Mutation; D015287:Neurokinin B / Q000235:genetics* / Q000378:metabolism*; D011627:Puberty / Q000502:physiology*; D018042:Receptors, Neurokinin-3 / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology*; D015320:Tachykinins / Q000235:genetics / Q000378:metabolism
D018042:Receptors, Neurokinin-3; D015320:Tachykinins; D007987:Gonadotropin-Releasing Hormone; D004399:Dynorphins; D015287:Neurokinin B