JOURNAL OF NEUROENDOCRINOLOGY, cilt.22, sa.7, ss.765-770, 2010 (SCI-Expanded)
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.