scholarly journals Kisspeptin-Gpr54 Signaling at the GnRH Neuron Is Necessary for Negative Feedback Regulation of Luteinizing Hormone Secretion in Female Mice

2014 ◽  
Vol 100 (2-3) ◽  
pp. 191-197 ◽  
Author(s):  
Shel-Hwa Yeo ◽  
Jenny Clarkson ◽  
Allan E. Herbison
Keyword(s):  
Luteinizing Hormone ◽  
Negative Feedback ◽  
Hormone Secretion ◽  
Feedback Regulation ◽  
Gnrh Neuron ◽  
Luteinizing Hormone Secretion ◽  
Negative Feedback Regulation ◽  
Female Mice

scholarly journals Endocrine Mechanisms of Puberty in Heifers: Estradiol Negative Feedback Regulation of Luteinizing Hormone Secretion 1

1984 ◽  
Vol 31 (2) ◽  
pp. 332-341 ◽  
Author(s):  
M. L. Day ◽  
K. Imakawa ◽  
M. Garcia-Winder ◽  
D. D. Zalesky ◽  
B. D. Schanbacher ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Negative Feedback ◽  
Hormone Secretion ◽  
Feedback Regulation ◽  
Luteinizing Hormone Secretion ◽  
Negative Feedback Regulation

EFFECT OF HYPOTHALAMIC DEAFFERENTATION ON THE CONTROL OF LUTEINIZING HORMONE SECRETION

1970 ◽  
Vol 46 (1) ◽  
pp. 1-7 ◽  
Author(s):  
S. TALEISNIK ◽  
M. E. VELASCO ◽  
J. J. ASTRADA
Keyword(s):  
Luteinizing Hormone ◽  
Negative Feedback ◽  
Positive Feedback ◽  
Hormone Secretion ◽  
Feedback Effect ◽  
Luteinizing Hormone Secretion ◽  
Ovarian Steroids ◽  
Medial Hypothalamus ◽  
Lh Release ◽  
Positive Feedback Effect

SUMMARY The influence that the interruption of the neural afferents to the hypothalamus exerts on ovulation and on the release of luteinizing hormone (LH) was studied in the rat. Animals with retrochiasmatic sections interrupting the neural connexions between the medial hypothalamus and the preoptic area (POA) showed constant oestrus and failed to ovulate. Animals in which the dorsal neural afferents to the POA were transected had oestrous cycles and ovulated normally. The positive feedback effect of progesterone on LH release in spayed animals primed either with 20 μg. oestradiol benzoate or 2·5 mg. testosterone propionate 3 days before was studied. Transection of the dorsal afferents to the POA favoured an increase in plasma LH, but in animals with retrochiasmatic sections the response was abolished. However, the negative feedback effect of ovarian steroids operated after both types of transection because an increase in plasma LH occurred after ovariectomy. It is concluded that the negative feedback effect of ovarian steroids acts on the medial hypothalamus which can maintain a tonic release of gonadotrophins in the absence of steroids. In contrast, the POA involved in the positive feedback effect of progesterone is concerned with the phasic release of LH.

scholarly journals Peripheral interleukin-1β inhibits arcuate kiss1 cells and LH pulses in female mice

2020 ◽  
Vol 246 (2) ◽  
pp. 149-160
Author(s):  
Katherine N Makowski ◽  
Michael J Kreisman ◽  
Richard B McCosh ◽  
Ali A Raad ◽  
Kellie M Breen
Keyword(s):  
Luteinizing Hormone ◽  
Cell Activation ◽  
Hormone Secretion ◽  
Receptor Activation ◽  
Gonadotropin Releasing Hormone ◽  
Interleukin 1Β ◽  
Luteinizing Hormone Secretion ◽  
Releasing Hormone ◽  
Female Mice ◽  
Neuroendocrine Function

Peripheral immune/inflammatory challenges rapidly disrupt reproductive neuroendocrine function. This inhibition is considered to be centrally mediated via suppression of gonadotropin-releasing hormone secretion, yet the neural pathway(s) for this effect remains unclear. We tested the hypothesis that interleukin-1β inhibits pulsatile luteinizing hormone secretion in female mice via inhibition of arcuate kisspeptin cell activation, a population of neurons considered to be the gonadotropin-releasing hormone pulse generator. In the first experiment, we determined that the inhibitory effect of peripheral interleukin-1β on luteinizing hormone secretion was enhanced by estradiol. We next utilized serial sampling and showed that interleukin-1β reduced the frequency of luteinizing hormone pulses in ovariectomized female mice treated with estradiol. The interleukin-1β-induced suppression of pulse frequency was associated with reduced kisspeptin cell activation, as determined by c-Fos coexpression, but not as a result of impaired responsiveness to kisspeptin challenge. Together, these data suggest an inhibitory action of interleukin-1β upstream of kisspeptin receptor activation. We next tested the hypothesis that estradiol enhances the activation of brainstem nuclei responding to interleukin-1β. We determined that the expression of interleukin-1 receptor was elevated within the brainstem following estradiol. Interleukin-1β induced c-Fos in the area postrema, ventrolateral medulla, and nucleus of the solitary tract; however, the response was not increased by estradiol. Collectively, these data support a neural mechanism whereby peripheral immune/inflammatory stress impairs reproductive neuroendocrine function via inhibition of kisspeptin cell activation and reduced pulsatile luteinizing hormone secretion. Furthermore, these findings implicate the influence of estradiol on peripherally mediated neural pathways such as those activated by peripheral cytokines.

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