Evidence map›Paper›PMID 20463213›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Altered GABAA receptor-mediated synaptic transmission disrupts the firing of gonadotropin-releasing hormone neurons in male mice under conditions that mimic steroid abuse.

Carlos A A Penatti, Matthew C Davis, Donna M Porter, Leslie P Henderson

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.5field-weighted citation impact, top 5% 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

24 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
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  5. Dominant Neuropeptide Cotransmission in Kisspeptin-GABA Regulation of GnRH Neuron Firing Driving Ovulation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
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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

4 authors at 1 institution in 1 country.

Carlos A A PenattiDepartment of Physiology, Dartmouth Medical School, Hanover, New Hampshire 03755, USA.
Matthew C Davis
Donna M Porter
Leslie P Henderson
Dartmouth College · US

Funding

PROJECT 3 - Steroid-Metabolic Interactions In the Control of GnRH NeuronsU54HD028934 · NICHD · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI MOENTER, SUZANNE M · 1998 to 2013
$16.5M
Steroid Regulation of Ion ChannelsR01DA014137 · NIDA · DARTMOUTH COLLEGE · PI HENDERSON, LESLIE P · 2001 to 2011
$3.0M
NICHD NIH HHS U54 HD028934NICHD NIH HHS U54 HD28934NIDA NIH HHS DA14137NIDA NIH HHS R01 DA014137
6 · The paper itself

Abstract

Gonadotropin-releasing hormone (GnRH) neurons are the central regulators of reproduction. GABAergic transmission plays a critical role in pubertal activation of pulsatile GnRH secretion. Self-administration of excessive doses of anabolic androgenic steroids (AAS) disrupts reproductive function and may have critical repercussions for pubertal onset in adolescent users. Here, we demonstrate that chronic treatment of adolescent male mice with the AAS 17alpha-methyltestosterone significantly decreased action potential frequency in GnRH neurons, reduced the serum gonadotropin levels, and decreased testes mass. AAS treatment did not induce significant changes in GABAA receptor subunit mRNA levels or alter the amplitude or decay kinetics of GABAA receptor-mediated spontaneous postsynaptic currents (sPSCs) or tonic currents in GnRH neurons. However, AAS treatment significantly increased action potential frequency in neighboring medial preoptic area (mPOA) neurons and GABAA receptor-mediated sPSC frequency in GnRH neurons. In addition, physical isolation of the more lateral aspects of the mPOA from the medially localized GnRH neurons abrogated the AAS-induced increase in GABAA receptor-mediated sPSC frequency and the decrease in action potential firing in the GnRH cells. Our results indicate that AAS act predominantly on steroid-sensitive presynaptic neurons within the mPOA to impart significant increases in GABAA receptor-mediated inhibitory tone onto downstream GnRH neurons, resulting in diminished activity of these pivotal mediators of reproductive function. These AAS-induced changes in central GABAergic circuits of the forebrain may significantly contribute to the disruptive actions of these drugs on pubertal maturation and the development of reproductive competence in male steroid abusers.

Indexed as

Action PotentialsAnabolic AgentsAndrogensAnimalsGonadotropin-Releasing HormoneGonadotropinsGreen Fluorescent ProteinsHypothalamo-Hypophyseal SystemMaleMethyltestosteroneMiceMice, TransgenicNeuronsPreoptic AreaPresynaptic TerminalsReceptors, GABA-AAnabolic AgentsAndrogensGonadotropin-Releasing HormoneGonadotropinsGreen Fluorescent ProteinsMethyltestosteroneReceptors, GABA-ARNA, Messenger

Identifiers

PMID20463213
PMCPMC2881304
OpenAlexW1985312657

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.