ArticlePloS one2012
Mice genetically depleted of brain serotonin display social impairments, communication deficits and repetitive behaviors: possible relevance to autism.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 2 of them syntheses that pooled it.
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Who cites it
79 citing papers in PubMed, 2 syntheses or guidelines pooled it, 142 citations in OpenAlex.
- A systematic-review of olfactory deficits in neurodevelopmental disorders: From mouse to human.Neuroscience and biobehavioral reviews · 2021Pooled it
- Hyperbaric oxygen therapy for people with autism spectrum disorder (ASD).The Cochrane database of systematic reviews · 2016Pooled it
- Serotonin deficiency caused by inactivation of Tph2 in mice leads to widespread sex-dependent changes in cerebral oxidative metabolic activity.Journal of neural transmission (Vienna, Austria : 1996) · 2026Article
- The Role of Serotonin in Brain Development: From Molecular Pathways to Neurodevelopmental Risk.Cellular and molecular neurobiology · 2026Review
- The gut microbiome shapes social behaviour across animal species.Nature reviews. Microbiology · 2026Review
- Revisiting the Role of Serotonin in Attention-Deficit Hyperactivity Disorder: New Insights from Preclinical and Clinical Studies.Clinical drug investigation · 2025Review
- Tryptophan hydroxylase 2 deficiency alters autism-related behavioural phenotypes in rats.Scientific reports · 2025Article
- A review of the effects of different types of social behaviors on the recruitment of neuropeptides and neurotransmitters in the nucleus accumbens.Frontiers in neuroendocrinology · 2025Review
- Central Serotonin Deficiency Impairs Recovery of Sensorimotor Abilities After Spinal Cord Injury in Rats.International journal of molecular sciences · 2025Article
- Review: Dopamine, Serotonin, and the Translational Neuroscience of Aggression in Autism Spectrum Disorder.JAACAP open · 2025Review
- Socio-affective communication in Tph2-deficient rat pups: communal nesting aggravates growth retardation despite ameliorating maternal affiliation deficits.Molecular autism · 2024Article
- Interaction of serotonin/GLP-1 circuitry in a dual preclinical model for psychiatric disorders and metabolic dysfunction.Psychiatry research · 2024Article
- Microbiota influence on behavior: Integrative analysis of serotonin metabolism and behavioral profile in germ-free mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Increasing histone acetylation improves sociability and restores learning and memory in KAT6B-haploinsufficient mice.The Journal of clinical investigation · 2024Article
- Serotonin drives aggression and social behaviors of laboratory male mice in a semi-natural environment.Frontiers in behavioral neuroscience · 2024Article
- SLC4A10 mutation causes a neurological disorder associated with impaired GABAergic transmission.Brain : a journal of neurology · 2023Article
- Neuroendocrine mechanisms contributing to the coevolution of sociality and communication.Frontiers in neuroendocrinology · 2023Review
- Maternal LPS Exposure Enhances the 5-HT Level in the Prefrontal Cortex of Autism-like Young Offspring.Brain sciences · 2023Article
- Current State of Modeling Human Psychiatric Disorders Using Zebrafish.International journal of molecular sciences · 2023Review
- Autism-like behaviors regulated by the serotonin receptor 5-HT2B in the dorsal fan-shaped body neurons of Drosophila melanogaster.European journal of medical research · 2022Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Autism is a complex neurodevelopmental disorder characterized by impaired reciprocal social interaction, communication deficits and repetitive behaviors. A very large number of genes have been linked to autism, many of which encode proteins involved in the development and function of synaptic circuitry. However, the manner in which these mutated genes might participate, either individually or together, to cause autism is not understood. One factor known to exert extremely broad influence on brain development and network formation, and which has been linked to autism, is the neurotransmitter serotonin. Unfortunately, very little is known about how alterations in serotonin neuronal function might contribute to autism. To test the hypothesis that serotonin dysfunction can contribute to the core symptoms of autism, we analyzed mice lacking brain serotonin (via a null mutation in the gene for tryptophan hydroxylase 2 (TPH2)) for behaviors that are relevant to this disorder. Mice lacking brain serotonin (TPH2-/-) showed substantial deficits in numerous validated tests of social interaction and communication. These mice also display highly repetitive and compulsive behaviors. Newborn TPH2-/- mutant mice show delays in the expression of key developmental milestones and their diminished preference for maternal scents over the scent of an unrelated female is a forerunner of more severe socialization deficits that emerge in weanlings and persist into adulthood. Taken together, these results indicate that a hypo-serotonin condition can lead to behavioral traits that are highly characteristic of autism. Our findings should stimulate new studies that focus on determining how brain hyposerotonemia during critical neurodevelopmental periods can alter the maturation of synaptic circuits known to be mis-wired in autism and how prevention of such deficits might prevent this disorder.
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Registered trials
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.