The developmental disruptions of serotonin signaling may involved in autism during early brain development
Abstract
Autism is a developmental disorder defined by the presence of a triad of communication, social and stereo typical behavioral characteristics with onset before 3years of age. In spite of the fact that there are potential environmental factors for autistic behavior, the dysfunction of serotonin during early development of the brain could be playing a role in this prevalence rise. Serotonin can modulate a number of developmental events, including cell division, neuronal migration, cell differentiation and synaptogenesis. Hyperserotonemia during fetal development results in the loss of serotonin terminals through negative feedback. The increased serotonin causes a decrease of oxytocin in the paraventricular nucleus of the hypothalamus and an increase in calcitonin gene-related peptide (CGRP) in the central nucleus of the amygdale, which are associated with social interactions and vital in autism. However, hyposerotonemia may be also relevant to the development of sensory as well as motor and cognitive faculties. And the paucity of placenta-derived serotonin should have potential importance when the pathogenesis of autism is considered. This review briefly summarized the developmental disruptions of serotonin signaling involved in the pathogenesis of autism during early development of the brain.
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There are indications that serotonergic signaling is affected during PFC development in ASD.
“There are also indications that serotonergic signaling is affected during PFC development [372].”
From Development of prefrontal cortex (2022) · cites this paper as [372]
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Between Dysbiosis, Maternal Immune Activation and Autism: Is There a Common Pathway?
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- Authors
- Yang, C.-J., Tan, H.-P., & Du, Y.-J.
- Affiliations
- East China Normal University (CN)
- Fudan University (CN)
- Corresponding author
- Yang, C.-J.
- Du, Y.-J.
- ORCID
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 2014-05
- Volume
- 267
- Pages
- 1-10
- ISSN
- 0306-4522 (ISSN-L)
- OpenAlex
- W1970406018
- Cited by
- 132
- References
- 121
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 12 · 2023: 17 · 2022: 18 · 2021: 13 · 2020: 13 · 2019: 7 · 2018: 5 · 2017: 9 · 2016: 7 · 2015: 12 · 2014: 3
- FWCI
- 1.00
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- East China Normal University (7119297K)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
- Keywords
- autism spectrum disorder, serotonin signaling, early brain development, fetal development, hyperserotonemia, serotonin terminals, oxytocin, paraventricular nucleus, calcitonin gene-related peptide, amygdala, neuronal migration, synaptogenesis, autism pathogenesis
- MeSH terms
- Autistic Disorder, Brain, Developmental Disabilities, Humans, Serotonin, Signal Transduction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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