Evidence map›Paper›PMID 32585679›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2020

Projection-specific deficits in synaptic transmission in adult Sapap3-knockout mice.

Lotfi C Hadjas, Michael M Schartner, Jennifer Cand, Meaghan C Creed, Vincent Pascoli, Christian Lüscher, Linda D Simmler

Abstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

25 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  17. The Sapap3Translational psychiatry · 2023
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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

7 authors.

Lotfi C HadjasDepartment of Basic Neurosciences, University of Geneva, Rue Michel-Servet 1, 1206, Geneva, Switzerland.
Michael M SchartnerDepartment of Basic Neurosciences, University of Geneva, Rue Michel-Servet 1, 1206, Geneva, Switzerland.
Jennifer CandDepartment of Basic Neurosciences, University of Geneva, Rue Michel-Servet 1, 1206, Geneva, Switzerland.
Meaghan C CreedDepartment of Basic Neurosciences, University of Geneva, Rue Michel-Servet 1, 1206, Geneva, Switzerland.ORCID http://orcid.org/0000-0002-9658-2601
Vincent PascoliDepartment of Basic Neurosciences, University of Geneva, Rue Michel-Servet 1, 1206, Geneva, Switzerland.
Christian LüscherDepartment of Basic Neurosciences, University of Geneva, Rue Michel-Servet 1, 1206, Geneva, Switzerland.ORCID http://orcid.org/0000-0001-7917-4596
Linda D SimmlerDepartment of Basic Neurosciences, University of Geneva, Rue Michel-Servet 1, 1206, Geneva, Switzerland. linda.simmler@unige.ch.ORCID http://orcid.org/0000-0003-3512-4057

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obsessive-compulsive disorder (OCD) is a circuit disorder involving corticostriatal projections, which play a role in motor control. The Sapap3-knockout (KO) mouse is a mouse model to study OCD and recapitulates OCD-like compulsion through excessive grooming behavior, with skin lesions appearing at advanced age. Deficits in corticostriatal control provide a link to the pathophysiology of OCD. However, there remain significant gaps in the characterization of the Sapap3-KO mouse, with respect to age, specificity of synaptic dysfunction, and locomotor phenotype. We therefore investigated the corticostriatal synaptic phenotype of Sapap3-KO mice using patch-clamp slice electrophysiology, in adult mice and with projection specificity. We also analyzed grooming across age and locomotor phenotype with a novel, unsupervised machine learning technique (MoSeq). Increased grooming in Sapap3-KO mice without skin lesions was age independent. Synaptic deficits persisted in adulthood and involved the projections from the motor cortices and cingulate cortex to the dorsolateral and dorsomedial striatum. Decreased synaptic strength was evident at the input from the primary motor cortex by reduction in AMPA receptor function. Hypolocomotion, i.e., slowness of movement, was consistently observed in Sapap3-KO mice. Our findings emphasize the utility of young adult Sapap3-KO mice to investigate corticostriatal synaptic dysfunction in motor control.

Indexed as

Nerve Tissue ProteinsObsessive-Compulsive DisorderAnimalsCorpus StriatumMiceMice, KnockoutSynaptic TransmissionNerve Tissue ProteinsSapap3 protein, mouse

Identifiers

PMID32585679
PMCPMC7547074

What OpenQuestion holds

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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.