Regulation of Gonadotropin-Releasing Hormone and Luteinizing Hormone Secretion by AMPA Receptors

1997 ◽  
Vol 66 (4) ◽  
pp. 246-253 ◽  
Author(s):  
Lin Ping ◽  
Virendra B. Mahesh ◽  
Ganapathy K. Bhat ◽  
Darrell W. Brann
Keyword(s):  
Luteinizing Hormone ◽  
Ampa Receptors ◽  
Hormone Secretion ◽  
Gonadotropin Releasing Hormone ◽  
Luteinizing Hormone Secretion ◽  
Releasing Hormone

scholarly journals Induction of final oocyte maturation in Cyprinidae fish by hypothalamic factors: a review

2009 ◽  
Vol 54 (No. 3) ◽  
pp. 97-110 ◽  
Author(s):  
P. Podhorec ◽  
J. Kouril
Keyword(s):  
Luteinizing Hormone ◽  
Oocyte Maturation ◽  
Hormone Secretion ◽  
Inhibitory Effect ◽  
Gonadotropin Releasing Hormone ◽  
Luteinizing Hormone Secretion ◽  
Releasing Hormone ◽  
Final Oocyte Maturation ◽  
In Captivity ◽  
Lh Secretion

Gonadotropin-releasing hormone in Cyprinidae as in other Vertebrates functions as a brain signal which stimulates the secretion of luteinizing hormone from the pituitary gland. Two forms of gonadotropin-releasing hormone have been identified in cyprinids, chicken gonadotropin-releasing hormone II and salmon gonadotropin-releasing hormone. Hypohysiotropic functions are fulfilled mainly by salmon gonadotropin-releasing hormone. The only known factor having an inhibitory effect on LH secretion in the family Cyprinidae is dopamine. Most cyprinids reared under controlled conditions exhibit signs of reproductive dysfunction, which is manifested in the failure to undergo final oocyte maturation and ovulation. In captivity a disruption of endogenous gonadotropin-releasing hormone stimulation occurs and sequentially that of luteinizing hormone, which is indispensible for the final phases of gametogenesis. In addition to methods based on the application of exogenous gonadotropins, the usage of a method functioning on the basis of hypothalamic control of final oocyte maturation and ovulation has become popular recently. The replacement of natural gonadotropin-releasing hormones with chemically synthesized gonadotropin-releasing hormone analogues characterized by amino acid substitutions at positions sensitive to enzymatic degradation has resulted in a centuple increase in the effectiveness of luteinizing hormone secretion induction. Combining gonadotropin-releasing hormone analogues with Dopamine inhibitory factors have made it possible to develop an extremely effective agent, which is necessary for the successful artificial reproduction of cyprinids.

Gonadotropin-Releasing Hormone-Stimulated Luteinizing Hormone Secretion by Perifused Pituitary Cells from Normal, Gonadectomized, and Testicular Feminized Rats*

Endocrinology ◽  
1990 ◽  
Vol 126 (6) ◽  
pp. 3022-3027 ◽  
Author(s):  
RICHARD J. KRIEG ◽  
JUDY M. BATSON ◽  
PAUL M. MARTHA ◽  
DENNIS W. MATT ◽  
RONALD L. SALISBURY ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Hormone Secretion ◽  
Gonadotropin Releasing Hormone ◽  
Pituitary Cells ◽  
Luteinizing Hormone Secretion ◽  
Releasing Hormone

scholarly journals Prostaglandins Mediate the Endotoxin-Induced Suppression of Pulsatile Gonadotropin-Releasing Hormone and Luteinizing Hormone Secretion in the Ewe*

Endocrinology ◽  
2000 ◽  
Vol 141 (3) ◽  
pp. 1050-1058 ◽  
Author(s):  
Thomas G. Harris ◽  
Deborah F. Battaglia ◽  
Martha E. Brown ◽  
Morton B. Brown ◽  
Nichole E. Carlson ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Hormone Secretion ◽  
Gonadotropin Releasing Hormone ◽  
Luteinizing Hormone Secretion ◽  
Releasing Hormone

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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