Faculty Opinions recommendation of Prostaglandin E2 release from astrocytes triggers gonadotropin-releasing hormone (GnRH) neuron firing via EP2 receptor activation.

2011 ◽  
Author(s):  
Allan Herbison
Keyword(s):  
Prostaglandin E2 ◽  
Receptor Activation ◽  
Gonadotropin Releasing Hormone ◽  
Gnrh Neuron ◽  
Neuron Firing ◽  
Releasing Hormone ◽  
Ep2 Receptor

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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