Evidence map›Paper›PMID 26838771›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2016

NgR1: A Tunable Sensor Regulating Memory Formation, Synaptic, and Dendritic Plasticity.

Tobias E Karlsson, Gabriella Smedfors, Alvin T S Brodin, Elin Åberg, Anna Mattsson, Isabelle Högbeck, Katrin Wellfelt, Anna Josephson, Stefan Brené, Lars Olson

Open access · hybridAbstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

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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

10 authors at 2 institutions in 2 countries.

Tobias E KarlssonDepartment of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Gabriella SmedforsDepartment of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Alvin T S BrodinDepartment of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Elin ÅbergDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden Present address: AstraZeneca R&D, AstraZeneca Translational Science Centre at Science for Life Laboratory, Solna, Sweden.
Anna MattssonDepartment of Neuroscience, Karolinska Institutet, Stockholm, Sweden Present address: The Swedish Council on Health Technology Assessment, Stockholm, Sweden.
Isabelle HögbeckDepartment of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Katrin WellfeltDepartment of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Anna JosephsonDepartment of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Stefan BrenéDepartment of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet, Stockholm, Sweden.
Lars OlsonDepartment of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Karolinska Institutet · SEScience for Life Laboratory · SE

Funding

Role of Nogo receptor in addictionR21DA030067 · NIDA · KAROLINSKA INSTITUTE · PI BRENE, STEFAN · 2010 to 2011
$266k
NIDA NIH HHS 5R21DA030067
6 · The paper itself

Abstract

Nogo receptor 1 (NgR1) is expressed in forebrain neurons and mediates nerve growth inhibition in response to Nogo and other ligands. Neuronal activity downregulates NgR1 and the inability to downregulate NgR1 impairs long-term memory. We investigated behavior in a serial behavioral paradigm in mice that overexpress or lack NgR1, finding impaired locomotor behavior and recognition memory in mice lacking NgR1 and impaired sequential spatial learning in NgR1 overexpressing mice. We also investigated a role for NgR1 in drug-mediated sensitization and found that repeated cocaine exposure caused stronger locomotor responses but limited development of stereotypies in NgR1 overexpressing mice. This suggests that NgR1-regulated synaptic plasticity is needed to develop stereotypies. Ex vivo magnetic resonance imaging and diffusion tensor imaging analyses of NgR1 overexpressing brains did not reveal any major alterations. NgR1 overexpression resulted in significantly reduced density of mature spines and dendritic complexity. NgR1 overexpression also altered cocaine-induced effects on spine plasticity. Our results show that NgR1 is a negative regulator of both structural synaptic plasticity and dendritic complexity in a brain region-specific manner, and highlight anterior cingulate cortex as a key area for memory-related plasticity.

Indexed as

LocomotionNeuronal PlasticityAnimalsBrainCocaineDendritesDiffusion Tensor ImagingFemaleGyrus CinguliMagnetic Resonance ImagingMaleMiceMice, KnockoutNogo Receptor 1Recognition, PsychologyRotarod Performance TestCocaineNogo Receptor 1Rtn4r protein, mousecocaine sensitizationdendritic structureNgR1spatial memoryspine plasticity

Identifiers

PMID26838771
PMCPMC4785958
OpenAlexW2260159226

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.