Evidence map›Paper›PMID 30447391›Full record

ArticleNeuroscience2018

Enhanced GABAergic Tonic Inhibition Reduces Intrinsic Excitability of Hippocampal CA1 Pyramidal Cells in Experimental Autoimmune Encephalomyelitis.

Laura G Kammel, Weizheng Wei, Shekib A Jami, Rhonda R Voskuhl, Thomas J O'Dell

Abstract read
In one paragraph

Article in Neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 37% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. GABACellular and molecular neurobiology · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Neurodegeneration in multiple sclerosis.WIREs mechanisms of disease · 2023
    Review
  8. Article
  9. Review
  10. Review
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.

Laura G KammelMolecular, Cellular, and Integrative Physiology Graduate Program, University of California, Los Angeles, Los Angeles, CA, United States; Multiple Sclerosis Program and Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States.
Weizheng WeiDepartment of Physiology, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States.
Shekib A JamiMolecular, Cellular, and Integrative Physiology Graduate Program, University of California, Los Angeles, Los Angeles, CA, United States; Department of Physiology, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States.
Rhonda R VoskuhlMultiple Sclerosis Program and Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States.
Thomas J O'DellDepartment of Physiology, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States; UCLA Integrative Center for Learning and Memory, Brain Research Institute, Los Angeles, CA, United States. Electronic address: todell@mednet.ucla.edu.
University of California, Los Angeles · US

Funding

Neuroendocrinology, Sex Differences, and ReproductionT32HD007228 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARNOLD, ARTHUR P · 1985 to 2015
$3.9M
Estrogen Receptor Beta-Targeted Treatment to Maintain Cognitive Function During MenopauseF31AG051381 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KAMMEL, LAURA · 2016 to 2017
$71k
NIA NIH HHS F31 AG051381NICHD NIH HHS T32 HD007228
6 · The paper itself

Abstract

Cognitive impairment (CI), a debilitating and pervasive feature of multiple sclerosis (MS), is correlated with hippocampal atrophy. Findings from postmortem MS hippocampi indicate that expression of genes involved in both excitatory and inhibitory neurotransmission are altered in MS, and although deficits in excitatory neurotransmission have been reported in the MS model experimental autoimmune encephalomyelitis (EAE), the functional consequence of altered inhibitory neurotransmission remains poorly understood. In this study, we used electrophysiological and biochemical techniques to examine inhibitory neurotransmission in the CA1 region of the hippocampus in EAE. We find that tonic, GABAergic inhibition is enhanced in CA1 pyramidal cells from EAE mice. Although plasma membrane expression of the GABA transporter GAT-3 was decreased in the EAE hippocampus, an increased surface expression of α5 subunit-containing GABA

Indexed as

AnimalsCA1 Region, HippocampalEncephalomyelitis, Autoimmune, ExperimentalGABA-A Receptor AntagonistsLong-Term PotentiationMiceNeural InhibitionPatch-Clamp TechniquesPyramidal CellsPyridazinesSynaptic TransmissionGABA-A Receptor AntagonistsgabazinePyridazinesexperimental autoimmune encephalomyelitishippocampusinhibitory synaptic transmissionintrinsic excitabilitylong-term potentiationmultiple sclerosistonic inhibition

Identifiers

PMID30447391
PMCPMC6289277
OpenAlexW2901587055

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.