Evidence map›Paper›PMID 34455539›Full record

ArticleMolecular neurobiology2021

Arhgap22 Disruption Leads to RAC1 Hyperactivity Affecting Hippocampal Glutamatergic Synapses and Cognition in Mice.

Anna Longatti, Luisa Ponzoni, Edoardo Moretto, Giorgia Giansante, Norma Lattuada, Maria Nicol Colombo, Maura Francolini, Mariaelvina Sala, Luca Murru, Maria Passafaro

Open access · hybridAbstract read
In one paragraph

Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Epigenetic markers of response to psychotherapy in obsessive-compulsive disorder.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. 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

10 authors at 2 institutions in 1 country.

Anna LongattiInstitute of Neuroscience, CNR, Milan, 20129, Italy.
Luisa PonzoniInstitute of Neuroscience, CNR, Milan, 20129, Italy.
Edoardo MorettoInstitute of Neuroscience, CNR, Milan, 20129, Italy.
Giorgia GiansanteInstitute of Neuroscience, CNR, Milan, 20129, Italy.
Norma LattuadaDepartment of Medical Biotechnology and Translational Medicine, Università Degli Studi Di Milano, 20129, Milan, Italy.
Maria Nicol ColomboDepartment of Medical Biotechnology and Translational Medicine, Università Degli Studi Di Milano, 20129, Milan, Italy.
Maura FrancoliniDepartment of Medical Biotechnology and Translational Medicine, Università Degli Studi Di Milano, 20129, Milan, Italy.
Mariaelvina SalaInstitute of Neuroscience, CNR, Milan, 20129, Italy.
Luca MurruInstitute of Neuroscience, CNR, Milan, 20129, Italy. luca.murru@in.cnr.it.
Maria PassafaroInstitute of Neuroscience, CNR, Milan, 20129, Italy. maria.passafaro@in.cnr.it.ORCID http://orcid.org/0000-0002-0045-5676
Neuroscience Institute · ITUniversity of Milan · IT

Funding

Fondazione Telethon GGP17283Ministero della Salute GR-2016-02361366Regione Lombardia 227333
6 · The paper itself

Abstract

Rho GTPases are a class of G-proteins involved in several aspects of cellular biology, including the regulation of actin cytoskeleton. The most studied members of this family are RHOA and RAC1 that act in concert to regulate actin dynamics. Recently, Rho GTPases gained much attention as synaptic regulators in the mammalian central nervous system (CNS). In this context, ARHGAP22 protein has been previously shown to specifically inhibit RAC1 activity thus standing as critical cytoskeleton regulator in cancer cell models; however, whether this function is maintained in neurons in the CNS is unknown. Here, we generated a knockout animal model for arhgap22 and provided evidence of its role in the hippocampus. Specifically, we found that ARHGAP22 absence leads to RAC1 hyperactivity and to an increase in dendritic spine density with defects in synaptic structure, molecular composition, and plasticity. Furthermore, arhgap22 silencing causes impairment in cognition and a reduction in anxiety-like behavior in mice. We also found that inhibiting RAC1 restored synaptic plasticity in ARHGAP22 KO mice. All together, these results shed light on the specific role of ARHGAP22 in hippocampal excitatory synapse formation and function as well as in learning and memory behaviors.

Indexed as

AnimalsAnxietyBehavior, AnimalCognitionDendritic SpinesGlutamic AcidGTPase-Activating ProteinsHippocampusMaze LearningMiceMice, KnockoutMotor ActivityNeuronal PlasticityNeuronsNeuropeptidesrac1 GTP-Binding ProteinGlutamic AcidGTPase-Activating ProteinsNeuropeptidesrac1 GTP-Binding ProteinRac1 protein, mouseARHGAP22Dendritic spinesHippocampusLearning and memorySynaptic plasticity

Identifiers

PMID34455539
PMCPMC8639580
OpenAlexW3196691939

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.