Evidence map›Paper›PMID 38802535›Full record

ArticleCommunications biology2024

Altered projection-specific synaptic remodeling and its modification by oxytocin in an idiopathic autism marmoset model.

Jun Noguchi, Satoshi Watanabe, Tomofumi Oga, Risa Isoda, Keiko Nakagaki, Kazuhisa Sakai, Kayo Sumida, Kohei Hoshino, Koichi Saito, Izuru Miyawaki and 6 more

Abstract read
In one paragraph

Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. 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

16 authors.

Jun NoguchiDepartment of Ultrastructural Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Japan. jnoguchi@ncnp.go.jp.ORCID 0000-0002-8350-791X
Satoshi WatanabeDepartment of Ultrastructural Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Japan.ORCID 0000-0001-9821-7598
Tomofumi OgaDepartment of Ultrastructural Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Japan.
Risa IsodaDepartment of Ultrastructural Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Japan.
Keiko NakagakiDepartment of Ultrastructural Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Japan.
Kazuhisa SakaiDepartment of Ultrastructural Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Japan.
Kayo SumidaEnvironmental Health Science Laboratory, Sumitomo Chemical Co., Ltd., Osaka, Japan.
Kohei HoshinoPreclinical Research Laboratories, Sumitomo Pharma Co., Ltd., Osaka, Japan.
Koichi SaitoEnvironmental Health Science Laboratory, Sumitomo Chemical Co., Ltd., Osaka, Japan.
Izuru MiyawakiPreclinical Research Laboratories, Sumitomo Pharma Co., Ltd., Osaka, Japan.
Eriko SuganoLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Iwate University, Morioka, Japan.ORCID 0000-0001-6732-717X
Hiroshi TomitaLaboratory of Visual Neuroscience, Graduate Course in Biological Sciences, Iwate University, Morioka, Japan.ORCID 0000-0003-1051-2301
Hiroaki MizukamiDivision of Genetic Therapeutics, Jichi Medical University, Shimotsuke, Japan.
Akiya WatakabeLaboratory for Molecular Analysis of Higher Brain Function, Center for Brain Science, RIKEN, Wako, Japan.
Tetsuo YamamoriLaboratory for Molecular Analysis of Higher Brain Function, Center for Brain Science, RIKEN, Wako, Japan.
Noritaka IchinoheDepartment of Ultrastructural Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Japan. nichino@ncnp.go.jp.ORCID 0000-0002-8323-4552

Funding

MEXT | Japan Society for the Promotion of Science (JSPS) JP18K06497MEXT | Japan Society for the Promotion of Science (JSPS) JP22K07363National Center of Neurology and Psychiatry (NCNP) 3-5
6 · The paper itself

Abstract

Alterations in the experience-dependent and autonomous elaboration of neural circuits are assumed to underlie autism spectrum disorder (ASD), though it is unclear what synaptic traits are responsible. Here, utilizing a valproic acid-induced ASD marmoset model, which shares common molecular features with idiopathic ASD, we investigate changes in the structural dynamics of tuft dendrites of upper-layer pyramidal neurons and adjacent axons in the dorsomedial prefrontal cortex through two-photon microscopy. In model marmosets, dendritic spine turnover is upregulated, and spines are generated in clusters and survived more often than in control marmosets. Presynaptic boutons in local axons, but not in commissural long-range axons, demonstrate hyperdynamic turnover in model marmosets, suggesting alterations in projection-specific plasticity. Intriguingly, nasal oxytocin administration attenuates clustered spine emergence in model marmosets. Enhanced clustered spine generation, possibly unique to certain presynaptic partners, may be associated with ASD and be a potential therapeutic target.

Indexed as

CallithrixDisease Models, AnimalNeuronal PlasticityOxytocinAnimalsAutism Spectrum DisorderAutistic DisorderAxonsDendritic SpinesFemaleMalePrefrontal CortexPresynaptic TerminalsPyramidal CellsSynapsesValproic AcidOxytocinValproic Acid

Identifiers

PMID38802535
PMCPMC11130163

What Socratic 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 Socratic graph.