Cited by 51Autism Spectrum Disorder ResearchGenetics and Neurodevelopmental DisordersNeurotransmitter Receptor Influence on Behavior

Serotonin neuron abnormalities in the BTBR mouse model of autism

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Guo, Yue‐Ping, Commons, Kathryn G.·2017·Autism Research

Abstract

The inbred mouse strain BTBR T+Itpr3tf/J (BTBR) is studied as a model of idiopathic autism because they are less social and more resistant to change than other strains. Forebrain serotonin receptors and the response to serotonin drugs are altered in BTBR mice, yet it remains unknown if serotonin neurons themselves are abnormal. In this study, we found that serotonin tissue content and the density of serotonin axons is reduced in the hippocampus of BTBR mice in comparison to C57BL/6J (C57) mice. This was accompanied by possible compensatory changes in serotonin neurons that were most pronounced in regions known to provide innervation to the hippocampus: the caudal dorsal raphe (B6) and the median raphe. These changes included increased numbers of serotonin neurons and hyperactivation of Fos expression. Metrics of serotonin neurons in the rostral 2/3 of the dorsal raphe and serotonin content of the prefrontal cortex were less impacted. Thus, serotonin neurons exhibit region‐dependent abnormalities in the BTBR mouse that may contribute to their altered behavioral profile.Autism Res2017, 10: 66–77. © 2016 International Society for Autism Research, Wiley Periodicals, Inc.

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  • BTBR mice have more serotonin-expressing neurons in the caudal portions of the median and dorsal raphe but decreased axon terminals in the hippocampal CA1, decreased adult neurogenesis in the dentate gyrus, upregulation of postnatal turnover of excitatory synapses in the anterior frontal cortex, and unaltered synaptic density and PSD thickness in the somatosensory cortex.

    “The presence of more serotonin-expressing neurons in the caudal portions of the median and dorsal raphe but decreased axon terminals in the hippocampal CA1 [134], decreased adult neurogenesis in the dentate gyrus [338], upregulation of postnatal turnover of excitatory synapses in the anterior frontal cortex [172], and unaltered synaptic density and PSD thickness in the somatosensory cortex [381]”

    From Autism spectrum disorder: neuropathology and animal models (2017) · cites this paper as [134]

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Authors
Guo, Y., & Commons, K. G.
Affiliations
Boston Children's Hospital (US)
Corresponding author
Commons, Kathryn G.
Venue
Autism Research
Publisher
Wiley
Published
2016-08
Volume
10
Issue
1
Pages
66-77
ISSN
  • 1939-3792 (ISSN-L)
  • 1939-3806
OpenAlex
W2476581217
Cited by
51
References
61
Citations by year
2026: 1 · 2025: 5 · 2024: 4 · 2023: 8 · 2022: 8 · 2021: 5 · 2020: 6 · 2019: 2 · 2018: 4 · 2017: 8
FWCI
2.97
Type
journal article
Language
en
Open access
Locations
  • Autism Research (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute on Drug Abuse (DA021801, HD036379)
Topics
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Keywords
serotonergic neurons, BTBR mice, autism spectrum disorder, hippocampus, dorsal raphe nucleus, median raphe, Fos expression, prefrontal cortex, serotonin receptors
MeSH terms
Animals, Autistic Disorder, Chromatography, High Pressure Liquid, Disease Models, Animal, Mice, Inbred C57BL, Mice, Inbred Strains, Neurons, Serotonin, Mice

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