Evidence map›Paper›PMID 26404876›Full record

ArticleNeuroscience2015

Increased excitability and excitatory synaptic transmission during in vitro ischemia in the neonatal mouse hippocampus.

S A Zanelli, K Rajasekaran, D K Grosenbaugh, J Kapur

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2015. 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
1.3field-weighted citation impact, top 24% 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, 30 citations in OpenAlex.

  1. Article
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  7. On the origin of ultraslow spontaneous NaJournal of neurophysiology · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Immediate and delayed decrease of long term potentiation and memory deficits after neonatal intermittent hypoxia.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2019
    Article
  12. Article
  13. Review
  14. Optimized Model of Cerebral IschemiaFrontiers in neuroscience · 2017
    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

4 authors at 1 institution in 1 country.

S A ZanelliDepartment of Pediatrics, University of Virginia, Charlottesville, VA, United States. Electronic address: sz5d@virginia.edu.
K RajasekaranDepartment of Neurology, University of Virginia, Charlottesville, VA, United States. Electronic address: karthik.rajasekaran@utsouthwestern.edu.
D K GrosenbaughDepartment of Neurology, University of Virginia, Charlottesville, VA, United States. Electronic address: dg5kd@virginia.edu.
J KapurDepartment of Neurology, University of Virginia, Charlottesville, VA, United States; Department of Neuroscience, University of Virginia, Charlottesville, VA, United States. Electronic address: jk8t@virginia.edu.
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
Effects of Nitric Oxide on Synaptic Transmission in the Neonatal HippocampusK08NS063118 · NINDS · UNIVERSITY OF VIRGINIA · PI ZANELLI, SANTINA AGNES · 2010 to 2014
$855k
NINDS NIH HHS 1 K08 NS063118-01A1NINDS NIH HHS K08 NS063118NINDS NIH HHS R01 NS040337NINDS NIH HHS R01 NS044370
6 · The paper itself

Abstract

objectiveThe present study tested the hypothesis that exposure to in vitro hypoxia-ischemia alters membrane properties and excitability as well as excitatory synaptic transmission of CA1 pyramidal neurons in the neonatal mouse.

methodsExperiments were conducted in hippocampal slices in P7-P9 C57Bl/6 mice using whole-cell patch clamp in current- and voltage-clamp mode. Passive membrane potential (Vm), input resistance (Rin) and active (action potential (AP) threshold and amplitude) membrane properties of CA1 pyramidal neurons were assessed at baseline, during 10 min in vitro ischemia (oxygen-glucose deprivation (OGD)) and during reoxygenation. Spontaneous and miniature excitatory post-synaptic currents (s and mEPSCs) were studied under similar conditions.

resultsOGD caused significant depolarization of CA1 pyramidal neurons as well as decrease in AP threshold and increase in AP amplitude. These changes were blocked by the application of tetrodotoxin (TTX), indicating Na(+) channels' involvement. Following 10 min of reoxygenation, significant membrane hyperpolarization was noted and it was associated with a decrease in Rin. AP threshold and amplitude returned to baseline during that stage. sEPSC and mEPSC frequency increased during both OGD and reoxygenation but their amplitude remained unchanged. Additionally, we found that OGD decreases Ih (hyperpolarization activated current) in CA1 neurons from neonatal mice and this effect persists during reoxygenation. SIGNIFICANCE: These results indicate that in vitro ischemia leads to changes in membrane excitability mediated by sodium and potassium channels. Further, it results in enhanced neurotransmitter release from presynaptic terminals. These changes are likely to represent one of the mechanisms of hypoxia/ischemia-mediated seizures in the neonatal period.

Indexed as

Excitatory Postsynaptic PotentialsMiniature Postsynaptic PotentialsAction PotentialsAnimalsAnimals, NewbornCA1 Region, HippocampalHypoxia-Ischemia, BrainMiceMice, Inbred C57BLPyramidal Cellselectrophysiologyexcitabilityexcitatory postsynaptic currentneonatal brainseizure

Identifiers

PMID26404876
PMCPMC4635675
OpenAlexW1768736801

What OpenQuestion holds

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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.