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A new mouse line with reduced GluA2 Q/R site RNA editing exhibits loss of dendritic spines, hippocampal CA1-neuron loss, learning and memory impairments and NMDA receptor-independent seizure…

Overview of attention for article published in Molecular Brain, February 2020
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About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • Among the highest-scoring outputs from this source (#35 of 1,181)
  • High Attention Score compared to outputs of the same age (91st percentile)
  • High Attention Score compared to outputs of the same age and source (96th percentile)

Mentioned by

news
3 news outlets
twitter
7 X users
facebook
1 Facebook page
wikipedia
1 Wikipedia page

Citations

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47 Dimensions

Readers on

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98 Mendeley
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Title
A new mouse line with reduced GluA2 Q/R site RNA editing exhibits loss of dendritic spines, hippocampal CA1-neuron loss, learning and memory impairments and NMDA receptor-independent seizure vulnerability
Published in
Molecular Brain, February 2020
DOI 10.1186/s13041-020-0545-1
Pubmed ID
Authors

Lyndsey M. Konen, Amanda L. Wright, Gordon A. Royle, Gary P. Morris, Benjamin K. Lau, Patrick W. Seow, Raphael Zinn, Luke T. Milham, Christopher W. Vaughan, Bryce Vissel

Abstract

Calcium (Ca2+)-permeable AMPA receptors may, in certain circumstances, contribute to normal synaptic plasticity or to neurodegeneration. AMPA receptors are Ca2+-permeable if they lack the GluA2 subunit or if GluA2 is unedited at a single nucleic acid, known as the Q/R site. In this study, we examined mice engineered with a point mutation in the intronic editing complementary sequence (ECS) of the GluA2 gene, Gria2. Mice heterozygous for the ECS mutation (named GluA2+/ECS(G)) had a ~ 20% reduction in GluA2 RNA editing at the Q/R site. We conducted an initial phenotypic analysis of these mice, finding altered current-voltage relations (confirming expression of Ca2+-permeable AMPA receptors at the synapse). Anatomically, we observed a loss of hippocampal CA1 neurons, altered dendritic morphology and reductions in CA1 pyramidal cell spine density. Behaviourally, GluA2+/ECS(G) mice exhibited reduced motor coordination, and learning and memory impairments. Notably, the mice also exhibited both NMDA receptor-independent long-term potentiation (LTP) and vulnerability to NMDA receptor-independent seizures. These NMDA receptor-independent seizures were rescued by the Ca2+-permeable AMPA receptor antagonist IEM-1460. In summary, unedited GluA2(Q) may have the potential to drive NMDA receptor-independent processes in brain function and disease. Our study provides an initial characterisation of a new mouse model for studying the role of unedited GluA2(Q) in synaptic and dendritic spine plasticity in disorders where unedited GluA2(Q), synapse loss, neurodegeneration, behavioural impairments and/or seizures are observed, such as ischemia, seizures and epilepsy, Huntington's disease, amyotrophic lateral sclerosis, astrocytoma, cocaine seeking behaviour and Alzheimer's disease.

X Demographics

X Demographics

The data shown below were collected from the profiles of 7 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 98 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 98 100%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 22 22%
Student > Ph. D. Student 13 13%
Researcher 12 12%
Student > Doctoral Student 4 4%
Unspecified 4 4%
Other 10 10%
Unknown 33 34%
Readers by discipline Count As %
Neuroscience 22 22%
Biochemistry, Genetics and Molecular Biology 14 14%
Agricultural and Biological Sciences 7 7%
Pharmacology, Toxicology and Pharmaceutical Science 5 5%
Unspecified 4 4%
Other 13 13%
Unknown 33 34%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 26. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 06 November 2022.
All research outputs
#1,411,580
of 24,762,960 outputs
Outputs from Molecular Brain
#35
of 1,181 outputs
Outputs of similar age
#32,679
of 365,262 outputs
Outputs of similar age from Molecular Brain
#3
of 53 outputs
Altmetric has tracked 24,762,960 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 94th percentile: it's in the top 10% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 1,181 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 7.0. This one has done particularly well, scoring higher than 97% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 365,262 tracked outputs that were published within six weeks on either side of this one in any source. This one has done particularly well, scoring higher than 91% of its contemporaries.
We're also able to compare this research output to 53 others from the same source and published within six weeks on either side of this one. This one has done particularly well, scoring higher than 96% of its contemporaries.