Evidence map›Paper›PMID 26733536›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2017

Mechanisms of Neuronal Silencing After Cortical Spreading Depression.

P M Sawant-Pokam, P Suryavanshi, J M Mendez, F E Dudek, K C Brennan

Open access · bronzeAbstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Spreading depolarization: A wave that precedes and drives cerebral ischemic cell death-Target for neuroprotection.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
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  11. Role of astrocytes connexins - pannexins in acute brain injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  12. Article
  13. Article
  14. Isoflurane lowers the cerebral metabolic rate of oxygen and prevents hypoxia during cortical spreading depolarizationJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    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

5 authors at 1 institution in 1 country.

P M Sawant-PokamDepartment of Neurology.
P SuryavanshiDepartment of Neurology.
J M MendezDepartment of Neurology.
F E DudekDepartment of Neurosurgery, University of Utah School of Medicine, Salt Lake City, UT, USA.
K C BrennanDepartment of Neurology.
University of Utah · US

Funding

Sensory plasticity in migraineR01NS085413 · NINDS · UNIVERSITY OF UTAH · PI BRENNAN, KEVIN CHRISTOPHER · 2013 to 2017
$1.7M
Tools for migraine drug developmentR21NS083010 · NINDS · UNIVERSITY OF UTAH · PI BRENNAN, KEVIN CHRISTOPHER · 2013 to 2014
$408k
NINDS NIH HHS R01 NS085413NINDS NIH HHS R21 NS083010
6 · The paper itself

Abstract

Cortical spreading depression (CSD) is associated with migraine, stroke, and traumatic brain injury, but its mechanisms remain poorly understood. One of the major features of CSD is an hour-long silencing of neuronal activity. Though this silencing has clear ramifications for CSD-associated disease, it has not been fully explained. We used in vivo whole-cell recordings to examine the effects of CSD on layer 2/3 pyramidal neurons in mouse somatosensory cortex and used in vitro recordings to examine their mechanism. We found that CSD caused a reduction in spontaneous synaptic activity and action potential (AP) firing that lasted over an hour. Both pre- and postsynaptic mechanisms contributed to this silencing. Reductions in frequency of postsynaptic potentials were due to a reduction in presynaptic transmitter release probability as well as reduced AP activity. Decreases in postsynaptic potential amplitude were due to an inhibitory shift in the ratio of excitatory and inhibitory postsynaptic currents. This inhibitory shift in turn contributed to the reduced frequency of APs. Thus, distinct but complementary mechanisms generate the long neuronal silence that follows CSD. These cellular changes could contribute to wider network dysfunction in CSD-associated disease, while the pre- and postsynaptic mechanisms offer separate targets for therapy.

Indexed as

Action PotentialsAnimalsCortical Spreading DepressionInhibitory Postsynaptic PotentialsMaleMice, Inbred C57BLNeuronsPatch-Clamp TechniquesSomatosensory Cortexcortical spreading depressionexcitation inhibition balancesomatosensorywhole-cell recording

Identifiers

PMID26733536
PMCPMC6317285
OpenAlexW2337776655

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.