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Serotonin transporter variant drives preventable gastrointestinal abnormalities in development and function.

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Summary

Serotonin transporter (SERT) variants impact gut function in autism spectrum disorder (ASD). Altered SERT activity affects gut development and function, potentially contributing to ASD-related gastrointestinal issues.

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Area of Science:

Neuroscience
Gastroenterology
Developmental Biology

Background:

Autism spectrum disorder (ASD) frequently co-occurs with gastrointestinal (GI) disturbances.
The relationship between gut dysfunction and core ASD features remains unclear.
Genetic variants in the serotonin transporter (SERT, SLC6A4) have been linked to ASD.

Purpose of the Study:

To investigate the role of serotonin transporter (SERT) activity in the development of GI defects associated with ASD.
To explore the link between SERT function, enteric nervous system development, and ASD-related behaviors.

Main Methods:

Utilized mouse models with altered SERT expression (Ala56 variant and SERT-deficient mice).
Assessed GI function, including transit time, peristalsis, and enteric nervous system development.
Investigated the effects of SERT modulation during development using pharmacological agents.

Main Results:

Mice with increased SERT activity (Ala56 variant) exhibited GI defects like hypoplastic enteric nervous system and slow transit.
SERT-deficient mice and those exposed to a SERT antagonist showed opposite GI phenotypes.
Developmental administration of a 5-HT4 agonist ameliorated GI issues in Ala56 mice, suggesting impaired 5-HT4 neurogenesis.

Conclusions:

Altered serotonin signaling during development, specifically through SERT, can lead to persistent GI dysfunction.
Disturbed SERT activity may contribute to both GI and behavioral aspects of ASD.
Further research is needed on the prenatal effects of SERT-targeting therapies.