Evidence map›Paper›PMID 39764171›Full record

ArticleFrontiers in neural circuits2024

Adult neurogenesis in the ventral hippocampus decreased among animal models of neurodevelopmental disorders.

Lihao Sun, Nobuhiko Ohashi, Takuma Mori, Yuka Mizuno, Weichen Zang, Qi Guo, Emi Kouyama-Suzuki, Yoshinori Shirai, Katsuhiko Tabuchi

Abstract read
In one paragraph

Article in Frontiers in neural circuits, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

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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

9 authors.

Lihao Sun *Department of Molecular and Cellular Physiology, Shinshu University School of Medicine, Matsumoto, Japan.
Nobuhiko Ohashi *Department of Molecular and Cellular Physiology, Shinshu University School of Medicine, Matsumoto, Japan.
Takuma Mori *Department of Molecular and Cellular Physiology, Shinshu University School of Medicine, Matsumoto, Japan.
Yuka MizunoDepartment of Molecular and Cellular Physiology, Shinshu University School of Medicine, Matsumoto, Japan.
Weichen ZangDepartment of Molecular and Cellular Physiology, Shinshu University School of Medicine, Matsumoto, Japan.
Qi GuoDepartment of Molecular and Cellular Physiology, Shinshu University School of Medicine, Matsumoto, Japan.
Emi Kouyama-SuzukiDepartment of Molecular and Cellular Physiology, Shinshu University School of Medicine, Matsumoto, Japan.
Yoshinori ShiraiDepartment of Molecular and Cellular Physiology, Shinshu University School of Medicine, Matsumoto, Japan.
Katsuhiko TabuchiDepartment of Molecular and Cellular Physiology, Shinshu University School of Medicine, Matsumoto, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by deficits in social interaction and communication, along with restricted and repetitive behaviors. Both genetic and environmental factors contribute to ASD, with prenatal exposure to valproic acid (VPA) and nicotine being linked to increased risk. Impaired adult hippocampal neurogenesis, particularly in the ventral region, is thought to play a role in the social deficits observed in ASD. Methods: In this study, we investigated social behavior and adult hippocampal neurogenesis in C57BL/6J mice prenatally exposed to VPA or nicotine, as well as in genetically modified ASD models, including IQSEC2 knockout (KO) and NLGN3-R451C knock-in (KI) mice. Sociability and social novelty preference were evaluated using a three-chamber social interaction test. Adult hippocampal neurogenesis was assessed by BrdU and DCX immunofluorescence to identify newborn and immature neurons. Results: VPA-exposed mice displayed significant deficits in social interaction, while nicotine-exposed mice exhibited mild impairment in social novelty preference. Both IQSEC2 KO and NLGN3-R451C KI mice demonstrated reduced adult neurogenesis, particularly in the ventral hippocampus, a region associated with social behavior and emotion. Across all ASD mouse models, a significant reduction in BrdU+/NeuN+ cells in the ventral hippocampus was observed, while dorsal hippocampal neurogenesis remained relatively unaffected. Similar reductions in DCX-positive cells were identified in VPA, nicotine, and NLGN3-R451C KI mice, indicating impaired proliferation or differentiation of neuronal progenitors. Discussion: These findings suggest that impaired adult neurogenesis in the ventral hippocampus is a common hallmark across ASD mouse models and may underlie social behavior deficits. This study provides insight into region-specific neurogenic alterations linked to ASD pathophysiology and highlights potential targets for therapeutic interventions.

Indexed as

Disease Models, AnimalHippocampusMice, Inbred C57BLNeurogenesisSocial BehaviorValproic AcidAnimalsAutism Spectrum DisorderDoublecortin ProteinFemaleMaleMiceMice, KnockoutNeurodevelopmental DisordersNicotinePregnancyDcx protein, mouseDoublecortin ProteinNicotineValproic Acidadult hippocampal neurogenesisautism spectrum disorderIQSEC2neuroligin 3prenatal nicotine exposurevalproic acid

Identifiers

PMID39764171
PMCPMC11700985

What Socratic 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 Socratic graph.