Evidence map›Paper›PMID 30079374›Full record

ArticleeNeuro

Estradiol Increases Glutamate and GABA Neurotransmission into GnRH Neurons via Retrograde NO-Signaling in Proestrous Mice during the Positive Estradiol Feedback Period.

Imre Farkas, Flóra Bálint, Erzsébet Farkas, Csaba Vastagh, Csaba Fekete, Zsolt Liposits

Open access · goldAbstract read
In one paragraph

Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.7field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Altered Electrophysiology and Transcriptome of GnRH Neurons in Middle-Aged Female Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  4. Review
  5. Review
  6. Cholinergic Control of GnRH Neuron Physiology and Luteinizing Hormone Secretion in Male Mice: Involvement of ACh/GABA Cotransmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Frontiers in endocrinology · 2021
    Article
  15. Article
  16. Review
  17. Article
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Imre FarkasLaboratory of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest H-1083, Hungary.ORCID 0000-0002-0159-4408
Flóra BálintLaboratory of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest H-1083, Hungary.
Erzsébet FarkasLaboratory of Integrative Neuroendocrinology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest H-1083, Hungary.
Csaba VastaghLaboratory of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest H-1083, Hungary.
Csaba FeketeLaboratory of Integrative Neuroendocrinology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest H-1083, Hungary.
Zsolt LipositsLaboratory of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest H-1083, Hungary.ORCID 0000-0002-3508-2750
HUN-REN Institute of Experimental Medicine · HUPázmány Péter Catholic University · HUTufts Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Surge release of gonadotropin-releasing hormone (GnRH) is essential in the activation of pituitary gonadal unit at proestrus afternoon preceded by the rise of serum 17β-estradiol (E2) level during positive feedback period. Here, we describe a mechanism of positive estradiol feedback regulation acting directly on GnRH-green fluorescent protein (GFP) neurons of mice. Whole-cell clamp and loose patch recordings revealed that a high physiological dose of estradiol (200 pM), significantly increased firing rate at proestrus afternoon. The mPSC frequency at proestrus afternoon also increased, whereas it decreased at metestrus afternoon and had no effect at proestrus morning. Inhibition of the estrogen receptor β (ERβ), intracellular blockade of the Src kinase and phosphatidylinositol 3 kinase (PI3K) and scavenge of nitric oxide (NO) inside GnRH neurons prevented the facilitatory estradiol effect indicating involvement of the ERβ/Src/PI3K/Akt/nNOS pathway in this fast, direct stimulatory effect. Immunohistochemistry localized soluble guanylate cyclase, the main NO receptor, in both glutamatergic and GABAergic terminals innervating GnRH neurons. Accordingly, estradiol facilitated neurotransmissions to GnRH neurons via both GABA

Indexed as

AnimalsEstradiolgamma-Aminobutyric AcidGlutamic AcidGonadotropin-Releasing HormoneMiceMice, Inbred C57BLMice, TransgenicNeuronsNitric OxideProestrusSignal TransductionSynaptic TransmissionEstradiolgamma-Aminobutyric AcidGlutamic AcidGonadotropin-Releasing HormoneNitric OxideGABAglutamateGnRH neuronpositive estradiol feedbackretrograde nitric oxide signallingslice electrophysiology

Identifiers

PMID30079374
PMCPMC6073979
OpenAlexW2884360231

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.