Effects of Orchidectomy and Testosterone Replacement on Numbers of Kisspeptin-, Neurokinin B-, and Dynorphin A-Immunoreactive Neurones in the Arcuate Nucleus of the Hypothalamus in Obese and Diabetic Rats

2017 ◽  
Vol 29 (2) ◽  
Author(s):  
M. Dudek ◽  
P. A. Kołodziejski ◽  
E. Pruszyńska-Oszmałek ◽  
K. Ziarniak ◽  
J. H. Sliwowska
Keyword(s):  
Arcuate Nucleus ◽  
Diabetic Rats ◽  
Testosterone Replacement ◽  
Dynorphin A ◽  
Neurokinin B

Effects of Ovariectomy and Sex Hormone Replacement on Numbers of Kisspeptin-, Neurokinin B- and Dynorphin A-immunoreactive Neurons in the Arcuate Nucleus of the Hypothalamus in Obese and Diabetic Rats

Neuroscience ◽  
2020 ◽  
Vol 451 ◽  
pp. 184-196
Author(s):  
Kamil Ziarniak ◽  
Paweł A. Kołodziejski ◽  
Ewa Pruszyńska-Oszmałek ◽  
Monika Dudek ◽  
Imre Kalló ◽  
...  
Keyword(s):  
Arcuate Nucleus ◽  
Hormone Replacement ◽  
Diabetic Rats ◽  
Sex Hormone ◽  
Dynorphin A ◽  
Neurokinin B

scholarly journals Neurokinin B Signaling in the Female Rat: a Novel Link Between Stress and Reproduction

Endocrinology ◽  
2014 ◽  
Vol 155 (7) ◽  
pp. 2589-2601 ◽  
Author(s):  
P. Grachev ◽  
X.F. Li ◽  
M.H. Hu ◽  
S.Y. Li ◽  
R.P. Millar ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
Arcuate Nucleus ◽  
Pulse Generator ◽  
Ovariectomized Rats ◽  
Female Rat ◽  
Dynorphin A ◽  
Receptor Antagonists ◽  
Neurokinin B ◽  
Hypothalamic Arcuate Nucleus ◽  
Systemic Stress

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.

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