Evidence map›Paper›PMID 25378156›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Prolonged deficits in parvalbumin neuron stimulation-evoked network activity despite recovery of dendritic structure and excitability in the somatosensory cortex following global ischemia in mice.

Yicheng Xie, Shangbin Chen, Yujin Wu, Timothy H Murphy

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

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  19. Optogenetic Approaches to Target Specific Neural Circuits in Post-stroke Recovery.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016
    Review
  20. Resolution of High-Frequency Mesoscale Intracortical Maps Using the Genetically Encoded Glutamate Sensor iGluSnFR.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    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 2 institutions in 2 countries.

Yicheng XieDepartment of Psychiatry, Kinsmen Laboratory of Neurological Research and Brain Research Centre, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada.
Shangbin ChenDepartment of Psychiatry, Kinsmen Laboratory of Neurological Research and Brain Research Centre, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada.
Yujin WuDepartment of Psychiatry, Kinsmen Laboratory of Neurological Research and Brain Research Centre, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada.
Timothy H MurphyDepartment of Psychiatry, Kinsmen Laboratory of Neurological Research and Brain Research Centre, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada thmurphy@mail.ubc.ca.
Neurological Research Institute · USUniversity of British Columbia · CA

Funding

Canadian Institutes of Health Research MOP-111009
6 · The paper itself

Abstract

Relatively few studies have examined plasticity of inhibitory neuronal networks following stroke in vivo, primarily due to the inability to selectively monitor inhibition. We assessed the structure of parvalbumin (PV) interneurons during a 5 min period of global ischemia and reperfusion in mice, which mimicked cerebral ischemia during cardiac arrest or forms of transient ischemic attack. The dendritic structure of PV-neurons in cortical superficial layers was rapidly swollen and beaded during global ischemia, but recovered within 5-10 min following reperfusion. Using optogenetics and a multichannel optrode, we investigated the function of PV-neurons in mouse forelimb somatosensory cortex. We demonstrated pharmacologically that PV-channelrhodopsin-2 (ChR2) stimulation evoked activation in layer IV/V, which resulted in rapid current sinks mediated by photocurrent and action potentials (a measure of PV-neuron excitability), which was then followed by current sources mediated by network GABAergic synaptic activity. During ischemic depolarization, the PV-ChR2-evoked current sinks (excitability) were suppressed, but recovered rapidly following reperfusion concurrent with repolarization of the DC-EEG. In contrast, the current sources reflecting GABAergic synaptic network activity recovered slowly and incompletely, and was coincident with the partial recovery of the forepaw stimulation-evoked current sinks in layer IV/V 30 min post reperfusion. Our in vivo data suggest that the excitability of PV inhibitory neurons was suppressed during global ischemia and rapidly recovered during reperfusion. In contrast, PV-ChR2 stimulation-evoked GABAergic synaptic network activity exhibited a prolonged suppression even ∼1 h after reperfusion, which could contribute to the dysfunction of sensation and cognition following transient global ischemia.

Indexed as

Action PotentialsInhibitory Postsynaptic PotentialsAnimalsCerebral InfarctionChannelrhodopsinsDendritesGABAergic NeuronsInterneuronsMiceMice, Inbred C57BLOptogeneticsParvalbuminsSomatosensory CortexChannelrhodopsinsParvalbuminsinhibitory synaptic transmissionoptogeneticsparvalbumin neuronreperfusionstroketwo-photon imaging

Identifiers

PMID25378156
PMCPMC6608365
OpenAlexW2011324056

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.