Evidence map›Paper›PMID 25852484›Full record

ArticleFrontiers in cellular neuroscience2015

Shank3-mutant mice lacking exon 9 show altered excitation/inhibition balance, enhanced rearing, and spatial memory deficit.

Jiseok Lee, Changuk Chung, Seungmin Ha, Dongmin Lee, Do-Young Kim, Hyun Kim, Eunjoon Kim

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed
13.1field-weighted citation impact, top 1% 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

108 citing papers in PubMed, 153 citations in OpenAlex.

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  11. Behavioral decline in Shank3Molecular autism · 2024
    Article
  12. Prefrontal cortical circuits in social behaviors: an overview.Journal of Zhejiang University. Science. B · 2024
    Review
  13. Behavioral regression in shank3Research square · 2024
    Article
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48 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Jiseok LeeDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology Daejeon, South Korea.
Changuk ChungDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology Daejeon, South Korea.
Seungmin HaDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology Daejeon, South Korea.
Dongmin LeeDepartment of Anatomy and Division of Brain Korea 21, Biomedical Science, College of Medicine, Korea University Seoul, South Korea.
Do-Young KimDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology Daejeon, South Korea.
Hyun KimDepartment of Anatomy and Division of Brain Korea 21, Biomedical Science, College of Medicine, Korea University Seoul, South Korea.
Eunjoon KimDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology Daejeon, South Korea ; Center for Synaptic Brain Dysfunctions, Institute for Basic Science Daejeon, South Korea.
Korea Advanced Institute of Science and Technology · KRKorea University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Shank3 is a postsynaptic scaffolding protein implicated in synapse development and autism spectrum disorders. The Shank3 gene is known to produce diverse splice variants whose functions have not been fully explored. In the present study, we generated mice lacking Shank3 exon 9 (Shank3 (Δ9) mice), and thus missing five out of 10 known Shank3 splice variants containing the N-terminal ankyrin repeat region, including the longest splice variant, Shank3a. Our X-gal staining results revealed that Shank3 proteins encoded by exon 9-containing splice variants are abundant in upper cortical layers, striatum, hippocampus, and thalamus, but not in the olfactory bulb or cerebellum, despite the significant Shank3 mRNA levels in these regions. The hippocampal CA1 region of Shank3 (Δ9) mice exhibited reduced excitatory transmission at Schaffer collateral synapses and increased frequency of spontaneous inhibitory synaptic events in pyramidal neurons. In contrast, prelimbic layer 2/3 pyramidal neurons in the medial prefrontal cortex displayed decreased frequency of spontaneous inhibitory synaptic events, indicating alterations in the ratio of excitation/inhibition (E/I ratio) in the Shank3 (Δ9) brain. These mice displayed a mild increase in rearing in a novel environment and mildly impaired spatial memory, but showed normal social interaction and repetitive behavior. These results suggest that ankyrin repeat-containing Shank3 splice variants are important for E/I balance, rearing behavior, and spatial memory.

Indexed as

autismE/I ratiohyperactivitymemoryShank3synaptic transmission

Identifiers

PMID25852484
PMCPMC4365696
OpenAlexW2004173167

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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.