Evidence map›Paper›PMID 27042284›Full record

ArticleMolecular autism2016

Brinp1(-/-) mice exhibit autism-like behaviour, altered memory, hyperactivity and increased parvalbumin-positive cortical interneuron density.

Susan R Berkowicz, Travis J Featherby, Zhengdong Qu, Aminah Giousoh, Natalie A Borg, Julian I Heng, James C Whisstock, Phillip I Bird

Open access · goldAbstract read
In one paragraph

Article in Molecular autism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 38 citations in OpenAlex.

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  18. Repurposing a pore: highly conserved perforin-like proteins with alternative mechanisms.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
  19. Article
  20. Consequences of acute NaNeurotoxicology · 2017
    Article
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

8 authors at 3 institutions in 1 country.

Susan R BerkowiczDepartment of Biochemistry and Molecular Biology, Monash University, Clayton, VIC 3800 Australia.
Travis J FeatherbyFlorey Institute of Neuroscience and Mental Health, Parkville, VIC 3052 Australia.
Zhengdong QuAustralian Regenerative Medicine Institute, Monash University, Clayton, VIC 3800 Australia.
Aminah GiousohDepartment of Biochemistry and Molecular Biology, Monash University, Clayton, VIC 3800 Australia.
Natalie A BorgDepartment of Biochemistry and Molecular Biology, Monash University, Clayton, VIC 3800 Australia.
Julian I HengAustralian Regenerative Medicine Institute, Monash University, Clayton, VIC 3800 Australia.
James C Whisstock *Department of Biochemistry and Molecular Biology, Monash University, Clayton, VIC 3800 Australia.
Phillip I Bird *Department of Biochemistry and Molecular Biology, Monash University, Clayton, VIC 3800 Australia.
Monash University · AUAustralian Regenerative Medicine Institute · AUFlorey Institute of Neuroscience and Mental Health · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBMP/RA-inducible neural-specific protein 1 (Brinp1) is highly conserved in vertebrates, and continuously expressed in the neocortex, hippocampus, olfactory bulb and cerebellum from mid-embryonic development through to adulthood.

methodsBrinp1 knock-out (Brinp1(-/-)) mice were generated by Cre-recombinase-mediated removal of the third exon of Brinp1. Knock-out mice were characterised by behavioural phenotyping, immunohistochemistry and expression analysis of the developing and adult brain.

resultsAbsence of Brinp1 during development results in a behavioural phenotype resembling autism spectrum disorder (ASD), in which knock-out mice show reduced sociability and changes in vocalisation capacity. In addition, Brinp1(-/-) mice exhibit hyper-locomotor activity, have impaired short-term memory, and exhibit poor reproductive success. Brinp1(-/-) mice show increased density of parvalbumin-expressing interneurons in the adult mouse brain. Brinp1(-/-) mice do not show signs of altered neural precursor proliferation or increased apoptosis during late embryonic brain development. The expression of the related neuronal migration genes Astn1 and Astn2 is increased in the brains of Brinp1(-/-) mice, suggesting that they may ameliorate the effects of Brinp1 loss.

conclusionsBrinp1 plays an important role in normal brain development and function by influencing neuronal distribution within the cortex. The increased cortical PV-positive interneuron density and altered behaviour of Brinp1(-/-) mice resemble features of a subset of human neurological disorders; namely autism spectrum disorder (ASD) and the hyperactivity aspect of attention deficit hyperactivity disorder (ADHD).

Indexed as

AnimalsAttention Deficit Disorder with HyperactivityAutism Spectrum DisorderBehavior, AnimalBrainCell Cycle ProteinsDisease Models, AnimalFemaleGenotypeGlycoproteinsInterneuronsMaleMemory, Short-TermMiceMice, Inbred C57BLMice, KnockoutAstn1 protein, mouseAstn2 protein, mouseBRINP1 protein, mouseCell Cycle ProteinsGlycoproteinsNerve Tissue ProteinsParvalbuminsAutism spectrum disorderBrinp1CortexHyperactivityInterneuronKnock-outNeurodevelopmentParvalbumin

Identifiers

PMID27042284
PMCPMC4818446
OpenAlexW2321595698

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.