Evidence map›Paper›PMID 23303941›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Synaptic plasticity at intrathalamic connections via CaV3.3 T-type Ca2+ channels and GluN2B-containing NMDA receptors.

Simone Astori, Anita Lüthi

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

28 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  10. CaHandbook of experimental pharmacology · 2023
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  14. Global genetic deletion of CaScientific reports · 2020
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  19. Genetic risk between theHereditas · 2018
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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

2 authors.

Simone AstoriDepartment of Fundamental Neurosciences, University of Lausanne, CH-1005 Lausanne, Switzerland. simone.astori@unil.ch
Anita Lüthi

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The T-type Ca(2+) channels encoded by the Ca(V)3 genes are well established electrogenic drivers for burst discharge. Here, using Ca(V)3.3(-/-) mice we found that Ca(V)3.3 channels trigger synaptic plasticity in reticular thalamic neurons. Burst discharge via Ca(V)3.3 channels induced long-term potentiation at thalamoreticular inputs when coactivated with GluN2B-containing NMDA receptors, which are the dominant subtype at these synapses. Notably, oscillatory burst discharge of reticular neurons is typical for sleep-related rhythms, suggesting that sleep contributes to strengthening intrathalamic circuits.

Indexed as

AnimalsCalcium Channels, T-TypeElectrophysiological PhenomenaExcitatory Postsynaptic PotentialsIn Vitro TechniquesMiceMice, Inbred C57BLMice, KnockoutNeuronal PlasticityReceptors, AMPAReceptors, N-Methyl-D-AspartateReticular FormationSynapsesSynaptic TransmissionThalamusCacna1i protein, mouseCalcium Channels, T-TypeNR2B NMDA receptorReceptors, AMPAReceptors, N-Methyl-D-Aspartate

Identifiers

PMID23303941
PMCPMC6704895

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.