Characterisation ofKiss1r(Gpr54)-Expressing Neurones in the Arcuate Nucleus of the Female Rat Hypothalamus

2017 ◽  
Vol 29 (2) ◽  
Author(s):  
S. Higo ◽  
N. Iijima ◽  
H. Ozawa
Endocrinology ◽  
2009 ◽  
Vol 150 (7) ◽  
pp. 3237-3244 ◽  
Author(s):  
Tamara Blutstein ◽  
Peter J. Baab ◽  
H. Ronald Zielke ◽  
Jessica A. Mong

Endocrinology ◽  
2014 ◽  
Vol 155 (7) ◽  
pp. 2589-2601 ◽  
Author(s):  
P. Grachev ◽  
X.F. Li ◽  
M.H. Hu ◽  
S.Y. Li ◽  
R.P. Millar ◽  
...  

Acute systemic stress disrupts reproductive function by inhibiting pulsatile gonadotropin secretion. The underlying mechanism involves stress-induced suppression of the GnRH pulse generator, the functional unit of which is considered to be the hypothalamic arcuate nucleus kisspeptin/neurokinin B/dynorphin A neurons. Agonists of the neurokinin B (NKB) receptor (NK3R) have been shown to suppress the GnRH pulse generator, in a dynorphin A (Dyn)-dependent fashion, under hypoestrogenic conditions, and Dyn has been well documented to mediate several stress-related central regulatory functions. We hypothesized that the NKB/Dyn signaling cascade is required for stress-induced suppression of the GnRH pulse generator. To investigate this ovariectomized rats, iv administered with Escherichia coli lipopolysaccharide (LPS) following intracerebroventricular pretreatment with NK3R or κ-opioid receptor (Dyn receptor) antagonists, were subjected to frequent blood sampling for hormone analysis. Antagonism of NK3R, but not κ-opioid receptor, blocked the suppressive effect of LPS challenge on LH pulse frequency. Neither antagonist affected LPS-induced corticosterone secretion. Hypothalamic arcuate nucleus NKB neurons project to the paraventricular nucleus, the major hypothalamic source of the stress-related neuropeptides CRH and arginine vasopressin (AVP), which have been implicated in the stress-induced suppression of the hypothalamic-pituitary-gonadal axis. A separate group of ovariectomized rats was, therefore, used to address the potential involvement of central CRH and/or AVP signaling in the suppression of LH pulsatility induced by intracerebroventricular administration of a selective NK3R agonist, senktide. Neither AVP nor CRH receptor antagonists affected the senktide-induced suppression of the LH pulse; however, antagonism of type 2 CRH receptors attenuated the accompanying elevation of corticosterone levels. These data indicate that the suppression of the GnRH pulse generator by acute systemic stress requires hypothalamic NKB/NK3R signaling and that any involvement of CRH therewith is functionally upstream of NKB.


1990 ◽  
Vol 52 (5) ◽  
pp. 527-536 ◽  
Author(s):  
Ricardo Zorrilla ◽  
Jacques Simard ◽  
Eric Rhéaume ◽  
Fernand Labrie ◽  
Georges Pelletier

2002 ◽  
Vol 76 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Sébastien Bouret ◽  
Vincent Prevot ◽  
Toru Takumi ◽  
Jean-Claude Beauvillain ◽  
Valérie Mitchell

Endocrinology ◽  
1993 ◽  
Vol 133 (2) ◽  
pp. 939-941 ◽  
Author(s):  
A Seltzer ◽  
K Tsutsumi ◽  
K Shigematsu ◽  
J M Saavedra

Endocrinology ◽  
2001 ◽  
Vol 142 (9) ◽  
pp. 4055-4065 ◽  
Author(s):  
Sebastien Bouret ◽  
Myriam Tran Van Chuoi-Mariot ◽  
Vincent Prevot ◽  
Dominique Croix ◽  
Toru Takumi ◽  
...  

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