Somatostatin Inhibition of Gonadotropin-Releasing Hormone Neurons in Female and Male Mice

Bhattarai, Janardhan P.; Kaszás, Attila; Park, Seon Ah; Yin, Hua; Park, Soo Joung; Herbison, Allan E.; Han, Seong Kyu; Ábrahám, István M.

doi:10.1210/en.2010-0148

Cited by 31 publications

(16 citation statements)

References 43 publications

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“…LPS also inhibits kisspeptin and dynorphin cell activation in the ARC and kisspeptin in the mPOA, and increases somatostatin activation in the VMN (Fergani et al 2013); and C Fergani, J E Routly, D N Jones, L C Pickavance, R F Smith and H Dobson (2011), unpublished data). Somatostatin is one of the most potent inhibitors of GNRH neurone excitability so far identified (Bhattarai et al 2010).…”

Section: Host Responses In the Brain Associated With Uterine Diseasementioning

confidence: 99%

Innate immunity and inflammation of the bovine female reproductive tract in health and disease

Sheldon¹,

Cronin²,

Healey³

et al. 2014

Reproduction

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100

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Mammalian reproductive physiology and the development of viviparity co-evolved with inflammation and immunity over millennia. Many inflammatory mediators contribute to paracrine and endocrine signalling, and the maintenance of tissue homeostasis in the female reproductive tract. However, inflammation is also a feature of microbial infections of the reproductive tract. Bacteria and viruses commonly cause endometritis, perturb ovarian follicle development and suppress the endocrine activity of the hypothalamus and pituitary in cattle. Innate immunity is an evolutionary ancient system that orchestrates host cell inflammatory responses aimed at eliminating pathogens and repairing damaged tissue. Pattern recognition receptors on host cells bind pathogen-associated molecular patterns and damage-associated molecular patterns, leading to the activation of intracellular MAPK and NFkB signalling pathways and the release of inflammatory mediators. Inflammatory mediators typically include the interleukin cytokines IL1b and IL6, chemokines such as IL8, interferons and prostaglandins. This review outlines the mechanisms of inflammation and innate immunity in the bovine female reproductive tract during health and disease condition.

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Section: Host Responses In the Brain Associated With Uterine Diseasementioning

confidence: 99%

Innate immunity and inflammation of the bovine female reproductive tract in health and disease

Sheldon¹,

Cronin²,

Healey³

et al. 2014

Reproduction

128

100

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“…A subpopulation of GnRH neurons expresses somatostatin receptor type 3 (Sstr3) in rodents [86,96,97], where the somatostatinergic appositions exert strong inhibition in mice [96]. Though Sstr2 was found to be the predominant form in both rats and mice, Sstr3 expression was detected only in the GnRH neurons of female rodents [97].…”

Section: Discussionmentioning

confidence: 99%

Differential Gene Expression in Gonadotropin-Releasing Hormone Neurons of Male and Metestrous Female Mice

et al. 2015

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Background: Gonadotropin-releasing hormone (GnRH) neurons play a pivotal role in the regulation of the hypothalamic-pituitary gonadal axis in a sex-specific manner. We hypothesized that the differences seen in reproductive functions of males and females are associated with a sexually dimorphic gene expression profile of GnRH neurons. Methods and Results: We compared the transcriptome of GnRH neurons obtained from intact metestrous female and male GnRH-green fluorescent protein transgenic mice. About 1,500 individual GnRH neurons from each sex were sampled with laser capture microdissection followed by whole-transcriptome amplification for gene expression profiling. Under stringent selection criteria (fold change >1.6, adjusted p value 0.01), Affymetrix Mouse Genome 430 PM array analysis identified 543 differentially expressed genes. Sexual dimorphism was most apparent in gene clusters associated with synaptic communication, signal transduction, cell adhesion, vesicular transport and cell metabolism. To validate microarray results, 57 genes were selected, and 91% of their differential expression was confirmed by real-time PCR. Similarly, 88% of microarray results were confirmed with PCR from independent samples obtained by patch pipette harvesting and pooling of 30 GnRH neurons from each sex. We found significant differences in the expression of genes involved in vesicle priming and docking (Syt1, Cplx1), GABAergic (Gabra3, Gabrb3, Gabrg2) and glutamatergic (Gria1, Grin1, Slc17a6) neurotransmission, peptide signaling (Sstr3, Npr2, Cxcr4) and the regulation of intracellular ion homeostasis (Cacna1, Cacnb1, Cacng5, Kcnq2, Kcnc1). Conclusion: The striking sexual dimorphism of the GnRH neuron transcriptome we report here contributes to a better understanding of the differences in cellular mechanisms of GnRH neurons in the two sexes.

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“…SST, which was also up-regulated in both groups of hens during the PS, is the main inhibitory hormone of the somatotropic axis but has been shown to inhibit GnRH neuron activity in mice [9].…”

Section: Overview Of Degsmentioning

confidence: 94%

Transcriptome analysis of the hypothalamus and pituitary of turkey hens with low and high egg production

Brady

Liu

Hicks

et al. 2020

Preprint

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Background: High egg producing hens (HEPH) show increased hypothalamic and pituitary gene expression related to hypothalamo-pituitary-gonadal (HPG) axis stimulation as well as increased in vitro responsiveness to gonadotropin releasing hormone (GnRH) stimulation in the pituitary when compared to low egg producing hens (LEPH). Transcriptome analysis was performed on hypothalamus and pituitary samples from LEPH and HEPH to identify novel regulators of HPG axis function. Results: In the hypothalamus and pituitary, 4644 differentially expressed genes (DEGs) were identified between LEPH and HEPH, with 2021 genes up-regulated in LEPH and 2623 genes up-regulated in HEPH. In LEPH, up-regulated genes showed enrichment of the hypothalamo-pituitary-thyroid (HPT) axis. Beta-estradiol was identified as an upstream regulator regardless of tissue. When LEPH and HEPH samples were compared, beta-estradiol was activated in HEPH in 3 of the 4 comparisons, which correlated to the number of beta-estradiol target genes up-regulated in HEPH. In in vitro pituitary cell cultures from LEPH and HEPH, thyroid hormone pretreatment negatively impacted gonadotropin subunit mRNA levels in cells from both LEPH and HEPH, with the effect being more prominent in HEPH cells. Additionally, the effect of estradiol pretreatment on gonadotropin subunit mRNA levels in HEPH cells was negative, whereas estradiol pretreatment increased gonadotropin subunit mRNA levels in LEPH cells.Conclusions: Up-regulation of the HPT axis in LEPH and upstream beta-estradiol activation in HEPH may play a role in regulating HPG axis function, and ultimately ovulation rates. Furthermore, thyroid hormone and estradiol pretreatment impacted gonadotropin mRNA levels following GnRH stimulation, with the inhibitory effects of thyroid hormone being more detrimental in HEPH and estradiol stimulatory effects being more prominent in LEPH. Differential responsiveness to thyroid hormone and estradiol pretreatment may be due to desensitization of target genes to thyroid hormone and estradiol in LEPH and HEPH, respectively, in response general up-regulation of the HPT axis in LEPH and of the HPG axis in HEPH. Further studies will be necessary to identify possible target gene desensitization mechanisms and elicit the full role that the HPT axis and beta-estradiol upstream regulation play in egg production rates in turkey hens.

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Somatostatin Inhibition of Gonadotropin-Releasing Hormone Neurons in Female and Male Mice

Cited by 31 publications

References 43 publications

Innate immunity and inflammation of the bovine female reproductive tract in health and disease

Innate immunity and inflammation of the bovine female reproductive tract in health and disease

Differential Gene Expression in Gonadotropin-Releasing Hormone Neurons of Male and Metestrous Female Mice

Transcriptome analysis of the hypothalamus and pituitary of turkey hens with low and high egg production

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