Evidence map›Paper›PMID 23392116›Full record

ArticleAmerican journal of physiology. Cell physiology2013

GABAergic synaptic inputs of locus coeruleus neurons in wild-type and Mecp2-null mice.

Xin Jin, Ningren Cui, Weiwei Zhong, Xiao-Tao Jin, Chun Jiang

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.9field-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

34 citing papers in PubMed, 49 citations in OpenAlex.

  1. Endogenous opioids and the development of the mammalian respiratory control network.American journal of physiology. Lung cellular and molecular physiology · 2025
    Review
  2. Article
  3. Neuronal diversity of neuropeptide signaling, including galanin, in the mouse locus coeruleus.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. GABAergic System Dysfunction in Autism Spectrum Disorders.Frontiers in cell and developmental biology · 2021
    Review
  11. Article
  12. Article
  13. Early Postnatal Treatment with Valproate InducesInternational journal of molecular sciences · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  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

5 authors at 1 institution in 1 country.

Xin JinDepartment of Biology, Georgia State University, Atlanta, GA 30302-4010, USA.
Ningren Cui
Weiwei Zhong
Xiao-Tao Jin
Chun Jiang
Georgia State University · US

Funding

Breathing disorders in a mouse model of Rett syndromeR01NS073875 · NINDS · GEORGIA STATE UNIVERSITY · PI JIANG, CHUN · 2011 to 2015
$1.6M
NINDS NIH HHS NS-073875NINDS NIH HHS R01 NS073875
6 · The paper itself

Abstract

Rett syndrome is an autism spectrum disorder resulting from defects in the gene encoding the methyl-CpG-binding protein 2 (MeCP2). Deficiency of the Mecp2 gene causes abnormalities in several systems in the brain, especially the norepinephrinergic and GABAergic systems. The norepinephrinergic neurons in the locus coeruleus (LC) modulate a variety of neurons and play an important role in multiple functions in the central nervous system. In Mecp2(-/Y) mice, defects in the intrinsic membrane properties of LC neurons have been identified, while how their synaptic inputs are affected remains unclear. Therefore, we performed these brain slice studies to demonstrate how LC neurons are regulated by GABAergic inputs and how such synaptic inputs are affected by Mecp2 knockout. In whole cell current clamp, the firing activity of LC neurons was strongly inhibited by the GABAA receptor agonist muscimol, accompanied by hyperpolarization and a decrease in input resistance. Such a postsynaptic inhibition was significantly reduced (by ~30%) in Mecp2(-/Y) mice. Post- and presynaptic GABABergic inputs were found in LC neurons, which were likely mediated by the G protein-coupled, Ba(2+)-sensitive K(+) channels. The postsynaptic GABABergic inhibition was deficient by ~50% in Mecp2 knockout mice. Although the presynaptic GABABergic modulation appeared normal, both frequency and amplitude of the GABAAergic mIPSCs were drastically decreased (by 30-40%) in Mecp2-null mice. These results suggest that the Mecp2 disruption causes defects in both post- and presynaptic GABAergic systems in LC neurons, impairing GABAAergic and GABABergic postsynaptic inhibition and decreasing the GABA release from presynaptic terminals.

Indexed as

AnimalsBaclofenFemaleGABA AntagonistsGABA-A Receptor AgonistsGABA-B Receptor AgonistsGABAergic Neuronsgamma-Aminobutyric AcidHumansLocus CoeruleusMaleMembrane PotentialsMethyl-CpG-Binding Protein 2MiceMice, Inbred C57BLMice, TransgenicBaclofenGABA AntagonistsGABA-A Receptor AgonistsGABA-B Receptor Agonistsgamma-Aminobutyric AcidMecp2 protein, mouseMethyl-CpG-Binding Protein 2MuscimolphaclofenPotassium Channel BlockersPotassium Channels, Inwardly RectifyingReceptors, GABA-AReceptors, GABA-BbrainstemGABAergiclocus coeruleusnoradrenalineRett syndrome

Identifiers

PMID23392116
PMCPMC3651605
OpenAlexW2125837222

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.