ArticleJournal of neurochemistry2017
16p11.2 deletion syndrome mice perseverate with active coping response to acute stress - rescue by blocking 5-HT2A receptors.
Article in Journal of neurochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Maternal separation disrupts noradrenergic control of adult coping behaviors.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Circuit mechanism underlying fragmented sleep and memory deficits in 16p11.2 deletion mouse model of autism.iScience · 2024Article
- The pleiotropic spectrum of proximal 16p11.2 CNVs.American journal of human genetics · 2024Review
- Progress towards understanding risk factor mechanisms in the development of autism spectrum disorders.Biochemical Society transactions · 2024Review
- Circuit mechanism underlying fragmented sleep and memory deficits in 16p11.2 deletion mouse model of autism.bioRxiv : the preprint server for biology · 2024Article
- Circuit mechanism underlying fragmented sleep and memory deficits in 16p11.2 deletion mouse model of autism.Research square · 2024Article
- Sleep disturbances in autism spectrum disorder: Animal models, neural mechanisms, and therapeutics.Neurobiology of sleep and circadian rhythms · 2023Review
- Serotonin Receptors as Therapeutic Targets for Autism Spectrum Disorder Treatment.International journal of molecular sciences · 2022Review
- Altered Serotonin 2A (5-HTFrontiers in pharmacology · 2022Article
- Systemic enhancement of serotonin signaling reverses social deficits in multiple mouse models for ASD.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- Sex-Specific Stress-Related Behavioral Phenotypes and Central Amygdala Dysfunction in a Mouse Model of 16p11.2 Microdeletion.Biological psychiatry global open science · 2021Article
- 16p11.2 deletion is associated with hyperactivation of human iPSC-derived dopaminergic neuron networks and is rescued by RHOA inhibition in vitro.Nature communications · 2021Article
- Article
- Comprehensive Behavioral Phenotyping of a 16p11.2 Del Mouse Model for Neurodevelopmental Disorders.Autism research : official journal of the International Society for Autism Research · 2020Article
- Drug-responsive autism phenotypes in the 16p11.2 deletion mouse model: a central role for gene-environment interactions.Scientific reports · 2020Article
- Serotonin abnormalities in Dravet syndrome mice before and after the age of seizure onset.Brain research · 2019Article
- p38α MAPK signaling drives pharmacologically reversible brain and gastrointestinal phenotypes in the SERT Ala56 mouse.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
In humans a chromosomal hemideletion of the 16p11.2 region results in variable neurodevelopmental deficits including developmental delay, intellectual disability, and features of autism spectrum disorder (ASD). Serotonin is implicated in ASD but its role remains enigmatic. In this study we sought to determine if and how abnormalities in serotonin neurotransmission could contribute to the behavioral phenotype of the 16p11.2 deletion syndrome in a mouse model (Del mouse). As ASD is frequently associated with altered response to acute stress and stress may exacerbate repetitive behavior in ASD, we studied the Del mouse behavior in the context of an acute stress using the forced swim test, a paradigm well characterized with respect to serotonin. Del mice perseverated with active coping (swimming) in the forced swim test and failed to adopt passive coping strategies with time as did their wild-type littermates. Analysis of monoamine content by HPLC provided evidence for altered endogenous serotonin neurotransmission in Del mice while there was no effect of genotype on any other monoamine. Moreover, we found that Del mice were highly sensitive to the 5-HT2A antagonists M100907, which at a dose of 0.1 mg/kg normalized their level of active coping and restored the gradual shift to passive coping in the forced swim test. Supporting evidence for altered endogenous serotonin signaling was provided by observations of additional ligand effects including altered forebrain Fos expression. Taken together, these observations indicate notable changes in endogenous serotonin signaling in 16p11.2 deletion mice and support the therapeutic utility of 5-HT2A receptor antagonists.
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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.