ArticleMolecular autism2015
Reduced isolation-induced pup ultrasonic communication in mouse pups lacking brain serotonin.
Article in Molecular autism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 78 citations in OpenAlex.
- Maternal exposure to titanium dioxide nanoparticles disrupts ultrasonic vocalization development in mouse offspring.Particle and fibre toxicology · 2026Article
- The role of the kynurenine pathway in the pathophysiology of autism-like phenotype induced by maternal inflammation in male mice.Neurobiology of disease · 2026Article
- Distinct early development trajectories in Nf1Journal of neurodevelopmental disorders · 2025Article
- Tryptophan hydroxylase 2 deficiency alters autism-related behavioural phenotypes in rats.Scientific reports · 2025Article
- Socio-affective communication in Tph2-deficient rat pups: communal nesting aggravates growth retardation despite ameliorating maternal affiliation deficits.Molecular autism · 2024Article
- Altered socio-affective communication and amygdala development in mice with protocadherin10-deficient interneurons.Open biology · 2024Article
- Serotonin drives aggression and social behaviors of laboratory male mice in a semi-natural environment.Frontiers in behavioral neuroscience · 2024Article
- Serotonin: A Bridge for Infant-mother Bonding.Neuroscience bulletin · 2023Article
- Neuroendocrine mechanisms contributing to the coevolution of sociality and communication.Frontiers in neuroendocrinology · 2023Review
- Prenatal SAMe Treatment Changes via Epigenetic Mechanism/s USVs in Young Mice and Hippocampal Monoamines Turnover at Adulthood in a Mouse Model of Social Hierarchy and Depression.International journal of molecular sciences · 2023Article
- 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
- Delineating a serotonin 1B receptor circuit for appetite suppression in mice.The Journal of experimental medicine · 2022Article
- Early Detection of Male-Predominant Phenotypes in the Pattern of Ultrasonic Vocalizations Emitted by Autism Spectrum Disorder Model (Brain sciences · 2022Article
- Autistic-like behavioral effects of prenatal stress in juvenile Fmr1 mice: the relevance of sex differences and gene-environment interactions.Scientific reports · 2022Article
- Biological Timing and Neurodevelopmental Disorders: A Role for Circadian Dysfunction in Autism Spectrum Disorders.Frontiers in neuroscience · 2021Review
- Male-specific alterations in structure of isolation call sequences of mouse pups with 16p11.2 deletion.Genes, brain, and behavior · 2020Article
- A recurrent PJA1 variant in trigonocephaly and neurodevelopmental disorders.Annals of clinical and translational neurology · 2020Article
- Specific profile of ultrasonic communication in a mouse model of neurodevelopmental disorders.Scientific reports · 2019Article
- Article
- Extreme enhancement or depletion of serotonin transporter function and serotonin availability in autism spectrum disorder.Pharmacological research · 2019Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSerotonin (5-hydroxytryptamine, 5-HT) is a key modulatory neurotransmitter in the mammalian central nervous system (CNS) that plays an important role as a developmental signal. Several lines of evidence associate altered 5-HT signaling with psychopathology in humans, particularly neurodevelopmental disorders such as autism spectrum disorders (ASD). ASD are characterized by persistent social and communication deficits along with stereotyped and repetitive patterns of behavior, with all symptoms emerging early during development.
methodsHere, we employed a mouse model devoid of brain 5-HT due to the lack of the gene encoding tryptophan hydroxylase 2 (Tph2), the initial and rate-limiting enzyme of 5-HT synthesis in the CNS. Tph2 null mutant (Tph2 (-/-) ) mice show normal prenatal development; however, they display for yet unknown reasons severe growth retardation during the first postnatal weeks. We investigated, therefore, whether Tph2 (-/-) mice display deficits in isolation-induced ultrasonic vocalizations (USV) as pups during early life. Isolation-induced USV are the most commonly studied behavioral measure to assess developmental delays and communication deficits in rodent models for ASD, particularly as they serve an important communicative function in coordinating mother-pup interactions.
resultsTph2 (-/-) mouse pups displayed a clear deficit in the emission of isolation-induced USV, as compared to heterozygous and wildtype littermates, exactly during growth retardation onset, including reduced call numbers and deficits in call clustering and temporal organization.
conclusionsThe ultrasonic communication impairment displayed by Tph2 (-/-) mouse pups is likely to result in a deficient mother-infant interaction, presumably contributing to their growth retardation phenotype, and represents a prominent feature relevant to ASD.
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