Evidence map›Paper›PMID 38943193›Full record

ArticleMolecular brain2024

Cerebellar damage with inflammation upregulates oxytocin receptor expression in Bergmann Glia.

Ayumu Inutsuka, Aisa Hattori, Masahide Yoshida, Yuki Takayanagi, Tatsushi Onaka

Abstract read
In one paragraph

Article in Molecular brain, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

5 authors.

Ayumu InutsukaDepartment of Physiology, Jichi Medical University, Shimotsuke, 323-0498, Japan. inutsuka@jichi.ac.jp.ORCID 0000-0001-6503-5501
Aisa HattoriDepartment of Physiology, Jichi Medical University, Shimotsuke, 323-0498, Japan.
Masahide YoshidaDepartment of Physiology, Jichi Medical University, Shimotsuke, 323-0498, Japan.
Yuki TakayanagiDepartment of Physiology, Jichi Medical University, Shimotsuke, 323-0498, Japan.
Tatsushi OnakaDepartment of Physiology, Jichi Medical University, Shimotsuke, 323-0498, Japan. tonaka@jichi.ac.jp.ORCID 0000-0001-5666-9035

Funding

Japan Society for the Promotion of Science 19K06910Japan Society for the Promotion of Science 20H03419Japan Society for the Promotion of Science 22K06487
6 · The paper itself

Abstract

The cerebellum plays an important role in cognitive and social functioning. Childhood damage in the cerebellum increases the risk of autism spectrum disorder. Cerebellar inflammation induces social avoidance in mice. Oxytocin regulates social relationship and expression pattern of the oxytocin receptor in the brain is related to social behaviors. However, the expression patterns of the oxytocin receptor in the cerebellum remain controversial. Here, we report that the expression patterns of the oxytocin receptor in the cerebellum are highly variable among knock-in transgenic lines. We used Oxtr-Cre knock-in mice combined with a fluorescent reporter line and found that oxytocin receptor expression in Bergmann glia was more variable than that in Purkinje cells. We found that physical damage with inflammation induced the selective upregulation of the oxytocin receptor in Bergmann glia. Our findings indicate high variability in oxytocin receptor expression in the cerebellum and suggest that the oxytocin receptor can affect neural processing in pathological conditions, such as inflammation.

Indexed as

CerebellumInflammationMice, TransgenicNeurogliaReceptors, OxytocinUp-RegulationAnimalsMaleMiceMice, Inbred C57BLPurkinje CellsReceptors, OxytocinBergmann gliaCerebellumInflammationOxytocinPurkinje cell

Identifiers

PMID38943193
PMCPMC11214225

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.