Evidence map›Paper›PMID 18499748›Full record

ArticleEndocrinology2008

The gonadotropin-releasing hormone (GnRH) neuronal population is normal in size and distribution in GnRH-deficient and GnRH receptor-mutant hypogonadal mice.

John C Gill, Brandon Wadas, Peilin Chen, Wendy Portillo, Andrea Reyna, Elisa Jorgensen, Shaila Mani, Gerald A Schwarting, Suzanne M Moenter, Stuart Tobet and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.7field-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

22 citing papers in PubMed, 36 citations in OpenAlex.

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  12. Fast scan cyclic voltammetry as a novel method for detection of real-time gonadotropin-releasing hormone release in mouse brain slices.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
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  18. Embryonic gonadotropin-releasing hormone signaling is necessary for maturation of the male reproductive axis.Proceedings of the National Academy of Sciences of the United States of America · 2010
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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

11 authors at 6 institutions in 1 country.

John C GillDivision of Endocrinology, Diabetes and Hypertension, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Brandon Wadas
Peilin Chen
Wendy Portillo
Andrea Reyna
Elisa Jorgensen
Shaila Mani
Gerald A Schwarting
Suzanne M Moenter
Stuart Tobet
Ursula B Kaiser
Baylor College of Medicine · USColorado State University · USHarvard University · USUniversity of Virginia · USBrigham and Women's Hospital · USUniversity of Massachusetts Chan Medical School · US

Funding

Cellular and Molecular bases for rhythmic GnRH releaseR01HD034860 · NICHD · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI MOENTER, SUZANNE M · 2002 to 2016
$4.8M
REPRODUCTIVE PHYSIOLOGY OF LUTROPIN SYNTHESISR01HD019938 · NICHD · JOSLIN DIABETES CENTER · PI KAISER, URSULA B. · 1985 to 2017
$3.9M
CELLULAR AND PHYSIOLOGICAL MECHANISMS IN REPRODUCTIONT32HD007382 · NICHD · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI MARSHALL, JOHN C · 1990 to 2009
$1.8M
Hormones, Neuronal Phosphoproteins and BehaviorR01MH057442 · NIMH · BAYLOR COLLEGE OF MEDICINE · PI MANI, SHAILAJA K · 2004 to 2008
$1.6M
Steroid Hormones Regulatory Mechanisms and BehaviorR01MH063954 · NIMH · BAYLOR COLLEGE OF MEDICINE · PI MANI, SHAILAJA K · 2002 to 2006
$1.5M
Migration of early olfactory neuronal progenitorsR01DC009034 · NIDCD · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SCHWARTING, GERALD A · 2007 to 2009
$906k
GENE THERAPY FOR RESCUE OF REPRODUCTIVE FUNCTIONR21HD050412 · NICHD · BRIGHAM AND WOMEN'S HOSPITAL · PI KAISER, URSULA B · 2005 to 2006
$368k
HORMONES, NEURONAL PHOSPHOPROTEINS AND BEHAVIORR29MH057442 · NIMH · BAYLOR COLLEGE OF MEDICINE · PI MANI, SHAILAJA K · 1998 to 2002
$295k
Direct and transsynaptic actions of GnRH on GnRH neuronsF32HD056765 · NICHD · UNIVERSITY OF VIRGINIA · PI CHEN, PEILIN · 2007 to 2008
$78k
NICHD NIH HHS F32 HD056765NICHD NIH HHS R01 HD019938NICHD NIH HHS R01 HD034860NICHD NIH HHS R01 HD19938NICHD NIH HHS R01 HD 34860NICHD NIH HHS R21 HD050412NICHD NIH HHS T32 HD007382NICHD NIH HHS T32 HD07382NIDCD NIH HHS DC009034NIDCD NIH HHS R01 DC009034NIMH NIH HHS MH57442NIMH NIH HHS MH63954NIMH NIH HHS R01 MH057442NIMH NIH HHS R01 MH063954NIMH NIH HHS R29 MH057442
6 · The paper itself

Abstract

Hypothalamic GnRH neurons are essential for initiation and regulation of reproductive function. In addition to pituitary gonadotrope stimulation, activity of GnRH through its receptor (GnRHR) has been suggested to include autocrine regulation of the GnRH neuron. Two hypogonadal mouse strains, the Gnrh1 mutant (hpg) mice and Gnrhr mutant mice were used to investigate the potential role of GnRH signaling in the proper development and maintenance of GnRH neurons. Immunocytochemical analysis of heterozygous hpg mice revealed a GnRH neuron population that was normal in size and distribution, indicating no effect from reduced Gnrh1 gene dosage on the neurons themselves. To visualize GnRH neurons in homozygous GnRH-deficient hpg mice, heterozygous hpg mice were crossed with GnRH-green fluorescent protein (GFP) transgenic mice with targeted expression of the GFP reporter gene in GnRH neurons. Analysis of forebrains of homozygous hpg/GFP-positive mice immunostained for GFP revealed a normal population size and appropriate distribution of GnRH neurons in hpg mice, with immunoreactive neuronal processes present at the median eminence. Similarly, adult mice deficient in functional GnRHR possessed a full complement of GnRH neurons in the basal forebrain that was indistinguishable from the distribution of GnRH neurons in their wild-type counterparts. Moreover, hpg/GFP neurons retained the ability to generate spontaneous bursts of action potential firing activity, suggesting that GnRH peptide is not required for this function. These data establish that autocrine-paracrine GnRH-signaling is not a prerequisite for the developmental migration of GnRH neurons into the brain or for the projection of GnRH neurosecretory axons.

Indexed as

AnimalsAutocrine CommunicationCell CountCell MovementCell SizeElectrophysiologyFemaleGonadotropin-Releasing HormoneGreen Fluorescent ProteinsHypogonadismMaleMiceMice, Inbred C3HMice, TransgenicModels, BiologicalMutant ProteinsGonadotropin-Releasing HormoneGreen Fluorescent ProteinsMutant ProteinsReceptors, LHRH

Identifiers

PMID18499748
PMCPMC2553368
OpenAlexW2115952749

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.