A social encounter drives gene expression changes linked to neuronal function, brain development, and related disorders in mice expressing the serotonin transporter Ala56 variant
Open accessAbstract
Multiple lines of evidence implicate the serotonin (5-HT) system in social function, including biomarker findings in autism spectrum disorder. In mice, knock-in of a rare Gly56Ala substitution in the serotonin transporter (SERT) causes elevated whole blood 5-HT levels, increased 5-HT clearance in the brain, and altered social and repetitive behavior. To further examine the molecular impact of this variant on social response, SERT Ala56 mutant mice and wildtype littermate controls were exposed to a social or non-social stimulus. We examined the differential activation of the prefrontal cortex, lateral amygdala, and medial amygdala, to social stimuli through RNA sequencing. Differentially expressed genes were enriched in axonal guidance signaling pathways, networks related to nervous system development and function, neurological and psychiatric disorders, and behavior. These identified pathways and networks may shed light on the molecular cascades underlying the impact of altered SERT function on social behavior.
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Mice expressing a gain-of-function SERT variant that decreases 5-HT levels exhibit altered basal firing of DR 5-HT neurons.
“as well as altered basal firing of DR 5-HT neurons [120,121].”
From Neural circuits regulating prosocial behaviors (2023) · cites this paper as [121]
Mice expressing a gain-of-function SERT variant that decreases 5-HT levels exhibit impaired sociability.
“mice expressing a gain-of-function SERT variant that decreases 5-HT levels exhibit impaired sociability”
From Neural circuits regulating prosocial behaviors (2023) · cites this paper as [121]
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Neural circuits regulating prosocial behaviors
Walsh, J. J., Christoffel, D. J., & Malenka, R. C. (2023) · Neuropsychopharmacology · doi:10.1038/s41386-022-01348-8 · Cited by 72 · see citing works
- Authors
- O’Reilly, K. C., Anacker, A. M. J., Rogers, T. D., Forsberg, C. G., Wang, J., Zhang, B., Blakely, R. D., & Veenstra-VanderWeele, J.
- Affiliations
- New York State Psychiatric Institute (US)
- Middle Tennessee State University (US)
- Medical University of South Carolina (US)
- Baylor College of Medicine (US)
- Vanderbilt University (US)
- Corresponding author
- Veenstra-VanderWeele, Jeremy
- Venue
- Neuroscience Letters
- Publisher
- Elsevier BV
- Published
- 2020-06
- Volume
- 730
- Pages
- 135027
- ISSN
- 0304-3940 (ISSN-L)
- PMC
- PMC7440397
- OpenAlex
- W3023093592
- Cited by
- 8
- References
- 25
- Citations by year
- 2024: 1 · 2023: 2 · 2022: 2 · 2021: 2 · 2020: 1
- FWCI
- 0.80
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neuroscience Letters (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
- Keywords
- serotonin transporter, serotonergic system, social behavior, autism spectrum disorder, gene expression changes, prefrontal cortex, lateral amygdala, medial amygdala, brain development, repetitive behavior, social encounters
- MeSH terms
- Autism Spectrum Disorder, Animals, Brain, Disease Models, Animal, Male, Neurons, Serotonin, Social Behavior, Gene Expression, Serotonin Plasma Membrane Transport Proteins, Mice
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