Evidence map›Paper›PMID 29802289›Full record

ArticleNature communications2018

The CaMKII/NMDA receptor complex controls hippocampal synaptic transmission by kinase-dependent and independent mechanisms.

Salvatore Incontro, Javier Díaz-Alonso, Jillian Iafrati, Marta Vieira, Cedric S Asensio, Vikaas S Sohal, Katherine W Roche, Kevin J Bender, Roger A Nicoll

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 103 papers.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

103 citing papers in PubMed, 170 citations in OpenAlex.

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  5. Inactivation of NMDAR and CaMKII signaling within the prelimbic cortex blocks incubated cocaine- and sucrose-craving.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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  9. Widely Used CaMKII Regulatory Segment Mutations Cause Tight Actinin Binding and Dendritic Spine Enlargement in Unstimulated Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
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43 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Salvatore IncontroDepartment of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA, 94158, USA. salvincontro@gmail.com.
Javier Díaz-AlonsoDepartment of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA, 94158, USA.
Jillian IafratiDepartment of Psychiatry, University of California, San Francisco, San Francisco, CA, 94158, USA.
Marta VieiraReceptor Biology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892, USA.
Cedric S AsensioDepartment of Biological Sciences, University of Denver, Denver, CO, 80208, USA.ORCID http://orcid.org/0000-0002-2284-0217
Vikaas S SohalDepartment of Psychiatry, University of California, San Francisco, San Francisco, CA, 94158, USA.
Katherine W RocheReceptor Biology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892, USA.
Kevin J BenderDepartment of Neurology, University of California, San Francisco, San Francisco, CA, 94158, USA.
Roger A NicollDepartment of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA, 94158, USA. roger.nicoll@ucsf.edu.
University of California, San Francisco · USNational Institutes of Health · USUniversity of Denver · US

Funding

Synaptic Plasticity Regulated by Stargazin-like gamma-8R01MH070957 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NICOLL, ROGER A · 2004 to 2019
$6.3M
The synaptic cleft and glutamate receptor traffickingR01MH117139 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NICOLL, ROGER A · 2018 to 2022
$2.9M
Cellular and synaptic mechanisms for dopaminergic modulation of prefrontal cortexR01MH100292 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SOHAL, VIKAAS SINGH · 2013 to 2017
$2.5M
Cellular mechanisms for dopaminergic control of learning in prefrontal cortexR01DA035913 · NIDA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BENDER, KEVIN J · 2013 to 2017
$1.7M
Formation of the Regulated Secretory Pathway: a View from the CytosolR01GM124035 · NIGMS · UNIVERSITY OF DENVER (COLORADO SEMINARY) · PI ASENSIO, CEDRIC STEPHANE · 2017 to 2021
$1.5M
Cellular Mechanisms Controlling the Formation of Large Dense Core VesiclesR15GM116096 · NIGMS · UNIVERSITY OF DENVER (COLORADO SEMINARY) · PI ASENSIO, CEDRIC STEPHANE · 2015 to 2015
$360k
NIDA NIH HHS R01 DA035913NIGMS NIH HHS R01 GM124035NIGMS NIH HHS R15 GM116096NIMH NIH HHS R01 MH070957NIMH NIH HHS R01 MH100292NIMH NIH HHS R01 MH117139
6 · The paper itself

Abstract

CaMKII is one of the most studied synaptic proteins, but many critical issues regarding its role in synaptic function remain unresolved. Using a CRISPR-based system to delete CaMKII and replace it with mutated forms in single neurons, we have rigorously addressed its various synaptic roles. In brief, basal AMPAR and NMDAR synaptic transmission both require CaMKIIα, but not CaMKIIβ, indicating that, even in the adult, synaptic transmission is determined by the ongoing action of CaMKIIα. While AMPAR transmission requires kinase activity, NMDAR transmission does not, implying a scaffolding role for the CaMKII protein instead. LTP is abolished in the absence of CaMKIIα and/or CaMKIIβ and with an autophosphorylation impaired CaMKIIα (T286A). With the exception of NMDAR synaptic currents, all aspects of CaMKIIα signaling examined require binding to the NMDAR, emphasizing the essential role of this receptor as a master synaptic signaling hub.

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Cell MembraneCRISPR-Cas SystemsFemaleHEK293 CellsHippocampusHumansLong-Term PotentiationMiceMice, KnockoutNeuronsPhosphorylationRatsReceptors, GlutamateReceptors, N-Methyl-D-Aspartatealpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid subtype glutamate receptor, humanCalcium-Calmodulin-Dependent Protein Kinase Type 2Receptors, GlutamateReceptors, N-Methyl-D-Aspartate

Identifiers

PMID29802289
PMCPMC5970233
OpenAlexW2804368056

What OpenQuestion holds

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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.