Evidence map›Paper›PMID 19699726›Full record

ArticleBrain research2009

Nitric oxide alters GABAergic synaptic transmission in cultured hippocampal neurons.

Santina Zanelli, Martha Naylor, Jaideep Kapur

Abstract read
In one paragraph

Article in Brain research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

14 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Antioxidants (Basel, Switzerland) · 2020
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  10. Neuronal nitric oxide synthase-dependent S-nitrosylation of gephyrin regulates gephyrin clustering at GABAergic synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  11. Article
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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

3 authors at 1 institution in 1 country.

Santina ZanelliDepartment of Pediatrics, Box 800386, University of Virginia, Charlottesville, VA 22908, USA. sz5d@virginia.edu
Martha Naylor
Jaideep Kapur
University of Virginia · US

Funding

TREATMENT OF STATUS EPILEPTICUSR01NS040337 · NINDS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI KAPUR, JAIDEEP · 2000 to 2021
$5.0M
Neurosteroid Regulation of SeizuresR01NS044370 · NINDS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI KAPUR, JAIDEEP · 2003 to 2017
$4.1M
NINDS NIH HHS R01 NS 040337NINDS NIH HHS R01 NS040337NINDS NIH HHS R01 NS 044370NINDS NIH HHS R01 NS044370
6 · The paper itself

Abstract

Nitric oxide (NO) production increases during hypoxia/ischemia-reperfusion in the immature brain and is associated with neurotoxicity. NO at physiologic concentrations has been shown to modulate GABAergic (gamma-aminobutyric acid) synaptic transmission in the adult brain. However, the effects of neurotoxic concentrations of NO (relevant to hypoxia-ischemia) on GABAergic synaptic transmission remain unknown. The present study tests the hypothesis that nNOS is expressed at GABAergic synapses and that exposure to neurotoxic concentrations of NO results in enhanced GABAergic synaptic transmission in cultured hippocampal neurons (days-in-vitro 10-14) prepared from fetal rats. Using double immunocytochemistry techniques, we were able to demonstrate that nNOS is co-localized to both presynaptic and postsynaptic markers of GABAergic synapses. The effects of NO on GABAergic synaptic transmission were then studied using whole cell patch-clamp electrophysiology. Spontaneous and miniature inhibitory postsynaptic currents (sIPSCS and mIPSCs) were recorded prior to and after exposure to 250 microM of the NO donor diethyleneamine/nitric oxide adduct (DETA-NO). Exposure to DETA-NO resulted in increased sIPSCs and mIPSCs frequency, indicating that neurotoxic concentrations of NO enhance GABAergic synaptic transmission in cultured hippocampal neurons. Because GABA synapses appear to be excitatory in the immature brain, this effect may contribute to overall enhanced synaptic transmission and hyperexcitability. We speculate that NO represents one of the mechanisms by which hypoxia-ischemia increases seizure susceptibility in the immature brain.

Indexed as

AnimalsCells, CulturedEpilepsygamma-Aminobutyric AcidHippocampusHypoxia-Ischemia, BrainImmunohistochemistryInhibitory Postsynaptic PotentialsNeuronsNitric OxideNitric Oxide DonorsNitric Oxide Synthase Type IPatch-Clamp TechniquesRatsSynaptic MembranesSynaptic Transmissiongamma-Aminobutyric AcidNitric OxideNitric Oxide DonorsNitric Oxide Synthase Type I

Identifiers

PMID19699726
PMCPMC2792990
OpenAlexW2084415293

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.