Evidence map›Paper›PMID 21143655›Full record

ReviewThe European journal of neuroscience2010

Contribution of glial-neuronal interactions to the neuroendocrine control of female puberty.

Sergio R Ojeda, Alejandro Lomniczi, Ursula Sandau

Open access · greenAbstract readReview
In one paragraph

Review in The European journal of neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
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  20. Development of gonadotropin-releasing hormone secretion and pituitary response.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    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

3 authors at 2 institutions in 1 country.

Sergio R OjedaDivision of Neuroscience, Oregon National Primate Research Center/Oregon Health Sciences University, 505 N.W., 185th Avenue, Beaverton, OR 97006, USA. ojedas@ohsu.edu
Alejandro Lomniczi
Ursula Sandau
Oregon National Primate Research Center · USOregon Health & Science University · US

Funding

YR 50 PROJ- ROBERTS PRIMATE ISLETP51RR000163 · NCRR · OREGON REGIONAL PRIMATE RESEARCH CENTER · PI FRUH, KLAUS J · 1985 to 2011
$140.8M
VASOACTIVE FACTORS IN ART CYCLES AND OVARIAN HYPERSTIMULATION SYNDROMEU54HD018185 · NICHD · OREGON REGIONAL PRIMATE RESEARCH CENTER · PI BETHEA, CYNTHIA LOUISE · 1999 to 2010
$13.8M
NEUROENDOCRINOLOGY OF PUBERTY AND SEXUAL DEVELOPMENTR01HD025123 · NICHD · OREGON REGIONAL PRIMATE RESEARCH CENTER · PI OJEDA, SERGIO R · 1990 to 2010
$3.9M
Molecular Specifiers of Neural Cell PlasticityR01MH065438 · NIMH · OREGON HEALTH & SCIENCE UNIVERSITY · PI OJEDA, SERGIO R · 2003 to 2006
$1.4M
REPRODUCTIVE STEROIDS AND EXPERIMENTAL STROKEK01RR000163 · NCRR · OREGON HEALTH AND SCIENCE UNIVERSITY · PI MURPHY, STEPHANIE J · 2000 to 2004
$479k
NCRR NIH HHS K01 RR000163NCRR NIH HHS P51 RR000163NCRR NIH HHS RR000163NICHD NIH HHS HD25123NICHD NIH HHS R01 HD025123NICHD NIH HHS U54 HD018185NICHD NIH HHS U54 HD18185NIMH NIH HHS R01 MH065438
6 · The paper itself

Abstract

Mammalian puberty is initiated by an increased pulsatile release of the neuropeptide gonadotropin-releasing hormone (GnRH) from hypothalamic neuroendocrine neurons. Although this increase is primarily set in motion by neuronal networks synaptically connected to GnRH neurons, glial cells contribute to the process via at least two mechanisms. One involves production of growth factors acting via receptors endowed with either serine-threonine kinase or tyrosine kinase activity. The other involves plastic rearrangements of glia-GnRH neuron adhesiveness. Growth factors of the epidermal growth factor family acting via erbB receptors play a major role in glia-to-GnRH neuron communication. In turn, neurons facilitate astrocytic erbB signaling via glutamate-dependent cleavage of erbB ligand precursors. The genetic disruption of erbB receptors delays female sexual development due to impaired erbB ligand-induced glial prostaglandin E(2) release. The adhesiveness of glial cells to GnRH neurons involves at least two different cell-cell communication systems endowed with both adhesive and intracellular signaling capabilities. One is provided by synaptic cell adhesion molecule (SynCAM1), which establishes astrocyte-GnRH neuron adhesiveness via homophilic interactions and the other involves the heterophilic interaction of neuronal contactin with glial receptor-like protein tyrosine phosphatase-β. These findings indicate that the interaction of glial cells with GnRH neurons involves not only secreted bioactive molecules, but also cell-surface adhesive proteins able to set in motion intracellular signaling cascades.

Indexed as

AnimalsEpidermal Growth FactorErb-b2 Receptor Tyrosine KinasesErbB ReceptorsFemaleGlutamic AcidGonadotropin-Releasing HormoneNeurogliaNeuronsNeurosecretory SystemsPubertyReceptor, ErbB-4Sexual MaturationSignal TransductionEpidermal Growth FactorErb-b2 Receptor Tyrosine KinasesErbB ReceptorsGlutamic AcidGonadotropin-Releasing HormoneReceptor, ErbB-4

Identifiers

PMID21143655
PMCPMC3058235
OpenAlexW1713476966

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.