Evidence map›Paper›PMID 37316943›Full record

ArticleMolecular autism2023

Shank2 identifies a subset of glycinergic neurons involved in altered nociception in an autism model.

Florian Olde Heuvel, Najwa Ouali Alami, Oumayma Aousji, Esther Pogatzki-Zahn, Peter K Zahn, Hanna Wilhelm, Dhruva Deshpande, Elmira Khatamsaz, Alberto Catanese, Sarah Woelfle and 8 more

Open access · goldAbstract read
In one paragraph

Article in Molecular autism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

6 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. 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

18 authors at 4 institutions in 3 countries.

Florian Olde Heuvel *Department of Neurology, Ulm University, Ulm, Germany.ORCID 0000-0002-1109-8969
Najwa Ouali Alami *Department of Neurology, Ulm University, Ulm, Germany.ORCID 0000-0001-7046-5581
Oumayma Aousji *Department of Neurology, Ulm University, Ulm, Germany.
Esther Pogatzki-ZahnDepartment of Anesthesiology, Intensive Care and Pain Medicine, University Hospital Münster, Münster, Germany.ORCID 0000-0003-0981-3940
Peter K ZahnDepartment of Anesthesiology, Intensive Care and Pain Medicine, University Hospital Münster, Münster, Germany.ORCID 0000-0002-3583-9645
Hanna WilhelmDepartment of Neurology, Ulm University, Ulm, Germany.
Dhruva DeshpandeDepartment of Biophysics, Ulm University, Ulm, Germany.ORCID 0000-0001-6769-6784
Elmira KhatamsazDepartment of Neurology, Ulm University, Ulm, Germany.
Alberto CataneseInstitute of Anatomy and Cell Biology, Ulm University, Ulm, Germany.ORCID 0000-0002-8266-4913
Sarah WoelfleInstitute of Anatomy and Cell Biology, Ulm University, Ulm, Germany.
Michael SchönInstitute of Anatomy and Cell Biology, Ulm University, Ulm, Germany.ORCID 0000-0002-8905-1810
Sanjay JainDepartment of Internal Medicine (Renal), Pathology and Immunology, Washington University School of Medicine, St. Louis, USA.
Stefanie GrabruckerInstitute of Anatomy and Cell Biology, Ulm University, Ulm, Germany.ORCID 0000-0001-6293-3760
Albert C LudolphDepartment of Neurology, Ulm University, Ulm, Germany.
Chiara VerpelliInstitute of Neuroscience, National Science Council, Milan, Italy.ORCID 0000-0003-2949-9725
Jens MichaelisDepartment of Biophysics, Ulm University, Ulm, Germany.ORCID 0000-0002-2739-4172
Tobias M Boeckers *Institute of Anatomy and Cell Biology, Ulm University, Ulm, Germany. tobias.boeckers@uni-ulm.de.ORCID 0000-0002-1486-8535
Francesco Roselli *Department of Neurology, Ulm University, Ulm, Germany. francesco.roselli@uni-ulm.de.ORCID 0000-0001-9935-6899
Universität Ulm · DEUniversity Hospital Münster · DENational Research Council · ITWashington University in St. Louis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutism Spectrum Disorders (ASD) patients experience disturbed nociception in the form of either hyposensitivity to pain or allodynia. A substantial amount of processing of somatosensory and nociceptive stimulus takes place in the dorsal spinal cord. However, many of these circuits are not very well understood in the context of nociceptive processing in ASD.

methodsWe have used a Shank2

resultsWe determined that Shank2 LIMITATIONS: Our investigation is limited to male mice, in agreement with the higher representation of ASD in males; therefore, caution should be applied to extrapolate the findings to females. Furthermore, ASD is characterized by extensive genetic diversity and therefore the findings related to Shank2 mutant mice may not necessarily apply to patients with different gene mutations. Since nociceptive phenotypes in ASD range between hyper- and hypo-sensitivity, diverse mutations may affect the circuit in opposite ways.

conclusionOur findings prove that Shank2 expression identifies a new subset of inhibitory interneurons involved in reducing the transmission of nociceptive stimuli and whose unchecked activation is associated with pain hypersensitivity. We provide evidence that dysfunction in spinal cord pain processing may contribute to the nociceptive phenotypes in ASD.

Indexed as

Autistic DisorderAnimalsFemaleHumansInterneuronsMaleMiceNerve Tissue ProteinsNeuronsNociceptionPainNerve Tissue ProteinsShank2 protein, mouseAutism spectrum disorderGlycinergic interneuronsNociceptionShank2Spinal cord

Identifiers

PMID37316943
PMCPMC10265811
OpenAlexW4380684164

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.