Evidence map›Paper›PMID 21917995›Full record

ArticleJournal of neurophysiology2011

Endocannabinoids and prostaglandins both contribute to GnRH neuron-GABAergic afferent local feedback circuits.

Katarzyna M Glanowska, Suzanne M Moenter

Abstract read
In one paragraph

Article in Journal of neurophysiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Endocannabinoid System and Metabolism: The Influences of Sex.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Review
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  11. Review
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  15. Article
  16. Endocannabinoids and the Endocrine System in Health and Disease.Handbook of experimental pharmacology · 2015
    Review
  17. Review
  18. Updates in reproduction coming from the endocannabinoid system.International journal of endocrinology · 2014
    Review
  19. Article
  20. 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

2 authors at 2 institutions in 1 country.

Katarzyna M GlanowskaNeuroscience Graduate Program, University of Virginia, Charlottesville, Virginia, USA.
Suzanne M Moenter
University of Michigan–Ann Arbor · USUniversity of Virginia · US

Funding

PROJECT 3 - Steroid-Metabolic Interactions In the Control of GnRH NeuronsU54HD028934 · NICHD · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI MARSHALL, JOHN C · 1998 to 2013
$16.5M
Cellular and Molecular bases for rhythmic GnRH releaseR01HD034860 · NICHD · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI MOENTER, SUZANNE M · 2002 to 2016
$4.8M
NICHD NIH HHS R01 HD034860NICHD NIH HHS R01 HD34860NICHD NIH HHS U54 HD28934
6 · The paper itself

Abstract

Gonadotropin-releasing hormone (GnRH) neurons form the final common pathway for central control of fertility. Regulation of GnRH neurons by long-loop gonadal steroid feedback through steroid receptor-expressing afferents such as GABAergic neurons is well studied. Recently, local central feedback circuits regulating GnRH neurons were identified. GnRH neuronal depolarization induces short-term inhibition of their GABAergic afferents via a mechanism dependent on metabotropic glutamate receptor (mGluR) activation. GnRH neurons are enveloped in astrocytes, which express mGluRs. GnRH neurons also produce endocannabinoids, which can be induced by mGluR activation. We hypothesized the local GnRH-GABA circuit utilizes glia-derived and/or cannabinoid mechanisms and is altered by steroid milieu. Whole cell voltage-clamp was used to record GABAergic postsynaptic currents (PSCs) from GnRH neurons before and after action potential-like depolarizations were mimicked. In GnRH neurons from ovariectomized (OVX) mice, this depolarization reduced PSC frequency. This suppression was blocked by inhibition of prostaglandin synthesis with indomethacin, by a prostaglandin receptor antagonist, or by a specific glial metabolic poison, together suggesting the postulate that prostaglandins, potentially glia-derived, play a role in this circuit. This circuit was also inhibited by a CB1 receptor antagonist or by blockade of endocannabinoid synthesis in GnRH neurons, suggesting an endocannabinoid element, as well. In females, local circuit inhibition persisted in androgen-treated mice but not in estradiol-treated mice or young ovary-intact mice. In contrast, local circuit inhibition was present in gonad-intact males. These data suggest GnRH neurons interact with their afferent neurons using multiple mechanisms and that these local circuits can be modified by both sex and steroid feedback.

Indexed as

EndocannabinoidsAction PotentialsAfferent PathwaysAnalysis of VarianceAndrogensAnimalsBrainCannabinoid Receptor ModulatorsDihydrotestosteroneDrug InteractionsElectric StimulationEstradiolEstrogensFemalegamma-Aminobutyric AcidGonadotropin-Releasing HormoneAndrogensCannabinoid Receptor ModulatorsDihydrotestosteroneEndocannabinoidsenhanced green fluorescent proteinEstradiolEstrogensgamma-Aminobutyric AcidGonadotropin-Releasing HormoneGreen Fluorescent ProteinsPiperidinesProstaglandinsPyrazolesRimonabant

Identifiers

PMID21917995
PMCPMC3234080
OpenAlexW2111112963

What OpenQuestion holds

Textmetadata
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.