ArticleFrontiers in endocrinology2011
Gliotransmission by prostaglandin e(2): a prerequisite for GnRH neuronal function?
Article in Frontiers in endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
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- The cyclooxygenase-expressing mesenchyme resists intestinal epithelial injury by paracrine signaling.Cell regeneration (London, England) · 2023Article
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- Puberty, A Sensitive Window of Hypothalamic Development and Plasticity.Endocrinology · 2021Review
- Beta-nerve growth factor stimulates spontaneous electrical activity of in vitro embryonic mouse GnRH neurons through a P75 mediated-mechanism.Scientific reports · 2020Article
- Activation of epidermal growth factor receptor signaling mediates cellular senescence induced by certain pro-inflammatory cytokines.Aging cell · 2020Article
- Emerging Roles for Immune Cells and MicroRNAs in Modulating the Response to Cardiac Injury.Journal of cardiovascular development and disease · 2019Review
- Adipose mTORC1 Suppresses Prostaglandin Signaling and Beige Adipogenesis via the CRTC2-COX-2 Pathway.Cell reports · 2018Article
- Downregulation of Deiodinase 3 is the earliest event in photoperiodic and photorefractory activation of the gonadotropic axis in seasonal hamsters.Scientific reports · 2017Article
- Prostaglandin E2-Induced COX-2 Expressions via EP2 and EP4 Signaling Pathways in Human LoVo Colon Cancer Cells.International journal of molecular sciences · 2017Article
- Derivation and Evaluation of Putative Adverse Outcome Pathways for the Effects of Cyclooxygenase Inhibitors on Reproductive Processes in Female Fish.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- Connexin 30 controls the extension of astrocytic processes into the synaptic cleft through an unconventional non-channel function.Neuroscience bulletin · 2014Article
- From precocious puberty to infertility: metabolic control of the reproductive function.Frontiers in endocrinology · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Over the past four decades it has become clear that prostaglandin E(2) (PGE(2)), a phospholipid-derived signaling molecule, plays a fundamental role in modulating the gonadotropin-releasing hormone (GnRH) neuroendocrine system and in shaping the hypothalamus. In this review, after a brief historical overview, we highlight studies revealing that PGE(2) released by glial cells such as astrocytes and tanycytes is intimately involved in the active control of GnRH neuronal activity and neurosecretion. Recent evidence suggests that hypothalamic astrocytes surrounding GnRH neuronal cell bodies may respond to neuronal activity with an activation of the erbB receptor tyrosine kinase signaling, triggering the release of PGE(2) as a chemical transmitter from the glia themselves, and, in turn, leading to the feedback regulation of GnRH neuronal activity. At the GnRH neurohemal junction, in the median eminence of the hypothalamus, PGE(2) is released by tanycytes in response to cell-cell signaling initiated by glial cells and vascular endothelial cells. Upon its release, PGE(2) causes the retraction of the tanycyte end-feet enwrapping the GnRH nerve terminals, enabling them to approach the adjacent pericapillary space and thus likely facilitating neurohormone diffusion from these nerve terminals into the pituitary portal blood. In view of these new insights, we suggest that synaptically associated astrocytes and perijunctional tanycytes are integral modulatory elements of GnRH neuronal function at the cell soma/dendrite and nerve terminal levels, respectively.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.