Evidence map›Paper›PMID 34453663›Full record

ArticleNeurochemical research2021

Shank3 Deficiency is Associated With Altered Profile of Neurotransmission Markers in Pups and Adult Mice.

Stanislava Bukatova, Emese Renczes, Alexandra Reichova, Johan Filo, Anna Sadlonova, Boris Mravec, Daniela Ostatnikova, Jan Bakos, Zuzana Bacova

Abstract read
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In one paragraph

Article in Neurochemical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.4field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Altered Structural Plasticity Mediated by mGlu and NMDA Receptors and Impaired Cognition in a Genetic ASD Model (Shank3The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
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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

9 authors at 3 institutions in 1 country.

Stanislava BukatovaBiomedical Research Center, Institute of Experimental Endocrinology, The Slovak Academy of Sciences, Dubravska cesta 9, 845 05, Bratislava, Slovakia.
Emese RenczesFaculty of Medicine, Institute of Molecular Biomedicine, Comenius University in Bratislava, Bratislava, Slovakia.
Alexandra ReichovaBiomedical Research Center, Institute of Experimental Endocrinology, The Slovak Academy of Sciences, Dubravska cesta 9, 845 05, Bratislava, Slovakia.
Johan FiloFaculty of Medicine, Institute of Molecular Biomedicine, Comenius University in Bratislava, Bratislava, Slovakia.
Anna SadlonovaBiomedical Research Center, Institute of Experimental Endocrinology, The Slovak Academy of Sciences, Dubravska cesta 9, 845 05, Bratislava, Slovakia.
Boris MravecBiomedical Research Center, Institute of Experimental Endocrinology, The Slovak Academy of Sciences, Dubravska cesta 9, 845 05, Bratislava, Slovakia.
Daniela OstatnikovaFaculty of Medicine, Institute of Physiology, Comenius University in Bratislava, Bratislava, Slovakia.
Jan BakosBiomedical Research Center, Institute of Experimental Endocrinology, The Slovak Academy of Sciences, Dubravska cesta 9, 845 05, Bratislava, Slovakia. j.bakos@savba.sk.ORCID http://orcid.org/0000-0001-6995-5460
Zuzana BacovaBiomedical Research Center, Institute of Experimental Endocrinology, The Slovak Academy of Sciences, Dubravska cesta 9, 845 05, Bratislava, Slovakia.
Slovak Academy of Sciences · SKComenius University Bratislava · SKInstitute of Experimental Endocrinology of the Slovak Academy of Sciences · SK

Funding

Agentúra Ministerstva Školstva, Vedy, Výskumu a Športu SR VEGA 2/0148/21Agentúra Ministerstva Školstva, Vedy, Výskumu a Športu SR VEGA 2/0155/20Agentúra na Podporu Výskumu a Vývoja APVV-15-0045Agentúra na Podporu Výskumu a Vývoja APVV-15-205
6 · The paper itself

Abstract

Alterations in the balance between excitation and inhibition, especially in the brain's critical developmental periods, are considered an integral part of the pathophysiology of autism. However, the precise mechanisms have not yet been established. SH3 and multiple Ankyrin repeat domains 3 (Shank3) deficient mice represent a well-established transgenic model of a neurodevelopmental disorder with autistic symptomatology. In this study, we characterize the consequences of Shank3 deficiency according to (1) expression of specific markers of different neuronal populations in pups and adult mice and (2) social behaviour and anxiety in adult mice. Our research found enhanced expression of serotonin transporter and choline acetyltransferase in the hippocampus and hypothalamus in Shank3-deficient pups. We demonstrated marked brain region differences in expression of excitatory glutamatergic markers in pups and adult Shank3 deficient mice. We also observed reduced expression of inhibitory GABAergic markers and GABA receptor subunits in several brain areas in both pups and adult Shank3 deficient mice. Further analysis of dopaminergic brain areas (nucleus accumbens, ventral tegmental area) revealed lower expression levels of GABAergic markers in adult Shank3 deficient mice. Adult Shank3

Indexed as

Disease Models, AnimalSocial BehaviorSynaptic TransmissionAnimalsAnimals, NewbornMaleMiceMice, Inbred C57BLMice, KnockoutMicrofilament ProteinsNerve Tissue ProteinsNeuronsMicrofilament ProteinsNerve Tissue ProteinsShank3 protein, mouseAnxietyAutismGABALocomotor activitySerotonin transporterShank3

Identifiers

PMID34453663
OpenAlexW3195741880

What OpenQuestion holds

Textmetadata
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.