Evidence map›Paper›PMID 22182308›Full record

ArticleBMC neuroscience2011

Kalirin-7 is necessary for normal NMDA receptor-dependent synaptic plasticity.

Fouad Lemtiri-Chlieh, Liangfang Zhao, Drew D Kiraly, Betty A Eipper, Richard E Mains, Eric S Levine

Open access · goldAbstract read
In one paragraph

Article in BMC neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

32 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  9. Targeting the Small GTPase Superfamily through Their Regulatory Proteins.Angewandte Chemie (International ed. in English) · 2020
    Review
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  18. Kalirin and Trio proteins serve critical roles in excitatory synaptic transmission and LTP.Proceedings of the National Academy of Sciences of the United States of America · 2016
    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

6 authors at 2 institutions in 2 countries.

Fouad Lemtiri-ChliehThe King Abdullah University of Science and Technology, Thuwal, Kingdom of Saudi Arabia.
Liangfang Zhao
Drew D Kiraly
Betty A Eipper
Richard E Mains
Eric S Levine
UConn Health · USKing Abdullah University of Science and Technology · SA

Funding

Dissecting the role of one neuronal RhoGEF amongst many: the Kalirin-7 null mouseR01DA023082 · NIDA · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI MAINS, RICHARD E · 2008 to 2012
$1.6M
Constructing a Conditional Kalirin Null MouseR21DA018274 · NIDA · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI MAINS, RICHARD E · 2004 to 2005
$290k
Kalirin-7 is essential in cocaine signaling: focus on nucleus accumbensF30DA026706 · NIDA · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI KIRALY, DREW · 2011 to 2013
$108k
NIDA NIH HHS DA-23082NIDA NIH HHS DA-26706NIDA NIH HHS R01 DA023082NIDA NIH HHS R21 DA018274
6 · The paper itself

Abstract

backgroundDendritic spines represent the postsynaptic component of the vast majority of excitatory synapses present in the mammalian forebrain. The ability of spines to rapidly alter their shape, size, number and receptor content in response to stimulation is considered to be of paramount importance during the development of synaptic plasticity. Indeed, long-term potentiation (LTP), widely believed to be a cellular correlate of learning and memory, has been repeatedly shown to induce both spine enlargement and the formation of new dendritic spines. In our studies, we focus on Kalirin-7 (Kal7), a Rho GDP/GTP exchange factor (Rho-GEF) localized to the postsynaptic density that plays a crucial role in the development and maintenance of dendritic spines both in vitro and in vivo. Previous studies have shown that mice lacking Kal7 (Kal7(KO)) have decreased dendritic spine density in the hippocampus as well as focal hippocampal-dependent learning impairments.

resultsWe have performed a detailed electrophysiological characterization of the role of Kal7 in hippocampal synaptic plasticity. We show that loss of Kal7 results in impaired NMDA receptor-dependent LTP and long-term depression, whereas a NMDA receptor-independent form of LTP is shown to be normal in the absence of Kal7.

conclusionsThese results indicate that Kal7 is an essential and selective modulator of NMDA receptor-dependent synaptic plasticity in the hippocampus.

Indexed as

AnimalsDendritic SpinesEnzyme InhibitorsFemaleGuanine Nucleotide Exchange FactorsHippocampusMaleMiceMice, Inbred C57BLMice, KnockoutNeuronal PlasticityOrgan Culture TechniquesReceptors, N-Methyl-D-AspartateSynaptic TransmissionEnzyme InhibitorsGuanine Nucleotide Exchange FactorsKALRN protein, mouseReceptors, N-Methyl-D-Aspartate

Identifiers

PMID22182308
PMCPMC3261125
OpenAlexW2021069596

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.