Evidence map›Paper›PMID 21592235›Full record

ReviewJournal of neuroendocrinology2012

17β-oestradiol regulation of gonadotrophin-releasing hormone neuronal excitability.

O K Rønnekleiv, M A Bosch, C Zhang

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of neuroendocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.0field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. 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
  2. Article
  3. Bisphenol A Activates Calcium Influx in Immortalized GnRH Neurons.International journal of molecular sciences · 2019
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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

3 authors at 1 institution in 1 country.

O K RønnekleivDepartment of Physiology and Pharmacology, Oregon Health & Science University, Portland, OR 97239-3098, USA. ronnekle@ohsu.edu
M A Bosch
C Zhang
Oregon Health & Science University · US

Funding

Sex Differences in the Control of FeedingR01DK068098 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI KELLY, MARTIN JEFFREY, RØNNEKLEIV, OLINE KARIN · 2005 to 2024
$7.1M
BETA ENDORPHIN NEURONS AND THE CONTROL OF HOMEOSTASISR01NS038809 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI KELLY, MARTIN JEFFREY · 1999 to 2018
$6.8M
Estrogen Modulation of Bursting Activity in GnRH NeuronsR01NS043330 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI RØNNEKLEIV, OLINE KARIN · 2004 to 2019
$5.5M
Beta Endorphin Neurons and the Control of HomeostasisR56NS038809 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI KELLY, MARTIN JEFFREY · 2009 to 2009
$481k
Crosstalk between Estrogen and Metabolic Hormone Signaling in Kisspeptin NeuronsR56DK068098 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI KELLY, MARTIN JEFFREY, RØNNEKLEIV, OLINE KARIN · 2020 to 2020
$262k
NIDDK NIH HHS DK68098NIDDK NIH HHS R01 DK068098NIDDK NIH HHS R56 DK068098NINDS NIH HHS NS38809NINDS NIH HHS NS43330NINDS NIH HHS R01 NS038809NINDS NIH HHS R01 NS043330NINDS NIH HHS R56 NS038809
6 · The paper itself

Abstract

17β-Oestradiol (E(2)) is essential for cyclical gonadotrophin-releasing hormone (GnRH) neuronal activity and secretion. In particular, E(2) increases the excitability of GnRH neurones during the afternoon of pro-oestrus in the rodent, which is associated with increased synthesis and secretion of GnRH. It is well established that E(2) regulates the activity of GnRH neurones through both presynaptic and postsynaptic mechanisms. E(2) significantly modulates the mRNA expression of numerous ion channels in GnRH neurones and alters the associated endogenous conductances, including potassium (K(ATP) , A-type) currents and low-voltage T-type and high-voltage L-type calcium currents. Notably, K(ATP) channels are critical for maintaining GnRH neurones in a hyperpolarised state for recruiting the T-type calcium channels, which are important for burst firing in GnRH neurones. In addition, there are other critical channels contributing to burst firing pattern, including the small conductance Ca(2+) -activated K(+) channels that may be modulated by E(2) . Despite these advances, the cellular mechanisms underlying the cyclical GnRH neuronal activity and GnRH release are largely unknown. Ultimately, the ensemble of both pre- and postsynaptic targets of the actions of E(2) will dictate the excitability and activity pattern of GnRH neurones.

Indexed as

Action PotentialsAnimalsCalcium Channels, T-TypeEstradiolGonadotropin-Releasing HormoneNeuronsCalcium Channels, T-TypeEstradiolGonadotropin-Releasing Hormone

Identifiers

PMID21592235
PMCPMC3572201
OpenAlexW1806370607

What OpenQuestion holds

Textmetadata
LicenceTDM
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.