Evidence map›Paper›PMID 36747195›Full record

ArticleMolecular brain2023

The distribution of neuroligin4, an autism-related postsynaptic molecule, in the human brain.

Akie Toya, Masahide Fukada, Eiko Aoki, Tohru Matsuki, Masashi Ueda, Shima Eda, Yoshio Hashizume, Akio Iio, Shigeo Masaki, Atsuo Nakayama

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

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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

10 authors at 2 institutions in 1 country.

Akie ToyaDepartment of Cellular Pathology, Institute for Developmental Research, Aichi Developmental Disability Center, Kasugai, 480-0392, Japan.
Masahide FukadaDepartment of Cellular Pathology, Institute for Developmental Research, Aichi Developmental Disability Center, Kasugai, 480-0392, Japan.
Eiko AokiDepartment of Cellular Pathology, Institute for Developmental Research, Aichi Developmental Disability Center, Kasugai, 480-0392, Japan.
Tohru MatsukiDepartment of Cellular Pathology, Institute for Developmental Research, Aichi Developmental Disability Center, Kasugai, 480-0392, Japan.
Masashi UedaDepartment of Cellular Pathology, Institute for Developmental Research, Aichi Developmental Disability Center, Kasugai, 480-0392, Japan.
Shima EdaDepartment of Cellular Pathology, Institute for Developmental Research, Aichi Developmental Disability Center, Kasugai, 480-0392, Japan.
Yoshio HashizumeInstitute for Medical Science of Aging, Aichi Medical University, Nagakute, 480-1195, Japan.
Akio IioDepartment of Cellular Pathology, Institute for Developmental Research, Aichi Developmental Disability Center, Kasugai, 480-0392, Japan.
Shigeo MasakiDepartment of Cellular Pathology, Institute for Developmental Research, Aichi Developmental Disability Center, Kasugai, 480-0392, Japan.
Atsuo NakayamaDepartment of Cellular Pathology, Institute for Developmental Research, Aichi Developmental Disability Center, Kasugai, 480-0392, Japan. atsuon@inst-hsc.jp.ORCID 0000-0003-1444-0800
Aichi Developmental Disability Center · JPAichi Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NLGN4X was identified as a single causative gene of rare familial nonsyndromic autism for the first time. It encodes the postsynaptic membrane protein Neuroligin4 (NLGN4), the functions and roles of which, however, are not fully understood due to the lack of a closely homologous gene in rodents. It has been confirmed only recently that human NLGN4 is abundantly expressed in the cerebral cortex and is localized mainly to excitatory synapses. However, the detailed histological distribution of NLGN4, which may have important implications regarding the relationships between NLGN4 and autistic phenotypes, has not been clarified. In this study, we raised specific monoclonal and polyclonal antibodies against NLGN4 and examined the distribution of NLGN4 in developing and developed human brains by immunohistochemistry. We found that, in the brain, NLGN4 is expressed almost exclusively in neurons, in which it has a widespread cytoplasmic pattern of distribution. Among various types of neurons with NLGN4 expression, we identified consistently high expression of NLGN4 in hypothalamic oxytocin (OXT)/vasopressin (AVP)-producing cells. Quantitative analyses revealed that the majority of OXT/AVP-producing neurons expressed NLGN4. NLGN4 signals in other large neurons, such as pyramidal cells in the cerebral cortex and hippocampus as well as neurons in the locus coeruleus and the raphe nucleus, were also remarkable, clearly contrasting with no or scarce signals in Purkinje cells. These data suggest that NLGN4 functions in systems involved in intellectual abilities, social abilities, and sleep and wakefulness, impairments of which are commonly seen in autism.

Indexed as

Autistic DisorderArginine VasopressinCell Adhesion Molecules, NeuronalHumansHypothalamusNeuronsOxytocinPhenotypeSynapsesArginine VasopressinCell Adhesion Molecules, NeuronalNLGN4X protein, humanOxytocinArginine-vasopressinASDImmunohistochemistryNLGN4OxytocinPeriventricular nucleusSupraoptic nucleus

Identifiers

PMID36747195
PMCPMC9903511
OpenAlexW4319310718

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.