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Surge‐Like Luteinising Hormone Secretion Induced by Retrochiasmatic Area NK 3R Activation is Mediated Primarily by Arcuate Kisspeptin Neurones in the Ewe
Author(s) -
Grachev P.,
Porter K. L.,
Coolen L. M.,
McCosh R. B.,
Connors J. M.,
Hileman S. M.,
Lehman M. N.,
Goodman R. L.
Publication year - 2016
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/jne.12393
Subject(s) - kisspeptin , endocrinology , medicine , neurokinin b , preoptic area , hypothalamus , biology , agonist , receptor , arcuate nucleus , luteinizing hormone , gonadotropin releasing hormone , estrous cycle , secretion , neuropeptide , hormone , substance p
The neuropeptides neurokinin B ( NKB ) and kisspeptin are potent stimulators of gonadotrophin‐releasing hormone (GnRH)/luteinsing hormone ( LH ) secretion and are essential for human fertility. We have recently demonstrated that selective activation of NKB receptors ( NK 3R) within the retrochiasmatic area ( RC h) and the preoptic area ( POA ) triggers surge‐like LH secretion in ovary‐intact ewes, whereas blockade of RC h NK 3R suppresses oestradiol‐induced LH surges in ovariectomised ewes. Although these data suggest that NKB signalling within these regions of the hypothalamus mediates the positive‐feedback effects of oestradiol on LH secretion, the pathway through which it stimulates Gn RH / LH secretion remains unclear. We proposed that the action of NKB on RC h neurones drives the LH surge by stimulating kisspeptin‐induced Gn RH secretion. To test this hypothesis, we quantified the activation of the preoptic/hypothalamic populations of kisspeptin neurones in response to POA or RC h administration of senktide by dual‐label immunohistochemical detection of kisspeptin and c‐Fos (i.e. marker of neuronal activation). We then administered the NK 3R agonist, senktide, into the RC h of ewes in the follicular phase of the oestrous cycle and conducted frequent blood sampling during intracerebroventricular infusion of the kisspeptin receptor antagonist Kp‐271 or saline. Our results show that the surge‐like secretion of LH induced by RC h senktide administration coincided with a dramatic increase in c‐Fos expression within arcuate nucleus ( ARC ) kisspeptin neurones, and was completely blocked by Kp‐271 infusion. We substantiate these data with evidence of direct projections of RC h neurones to ARC kisspeptin neurones. Thus, NKB ‐responsive neurones in the RC h act to stimulate Gn RH secretion by inducing kisspeptin release from KND y neurones.

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