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Updated: Jul 8, 2026
Rapid In Situ Hybridization using Oligonucleotide Probes on Paraformaldehyde-prefixed Brain of Rats with Serotonin Syndrome
Published on: September 23, 2015
Targeting the murine serotonin transporter: insights into human neurobiology
Dennis L Murphy1, Klaus-Peter Lesch
1Laboratory of Clinical Science, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892, USA. DennisMurphy@mail.nih.gov
Abstract:
Mutations resulting in reduced or completely abrogated serotonin-transporter (SERT) function in mice have led to the identification of more than 50 different phenotypic changes, ranging from increased anxiety and stress-related behaviours to gut dysfunction, bone weakness and late-onset obesity with metabolic syndrome. These multiple effects, which can be amplified by gene-environment and gene-gene interactions, are primarily attributable to altered intracellular and extracellular serotonin concentrations during development and adulthood. Much of the human data relating to altered expression of the gene that encodes SERT are based on genetic-association findings or correlations and are therefore not as robust as the experimental mouse results. Nevertheless, SERT-function-modifying gene variants in humans apparently produce many phenotypes that are similar to those that manifest themselves in mice.
Insights
Reduced serotonin-transporter (SERT) function in mice causes over 50 diverse health issues, including anxiety and metabolic syndrome. Human gene variants show similar effects, highlighting SERT
Area of Science:
- Neuroscience
- Genetics
- Metabolic Disorders
Background:
- The serotonin-transporter (SERT) regulates serotonin levels, impacting various physiological processes.
- Mutations affecting SERT function are linked to a wide array of phenotypic changes.
Purpose of the Study:
- To investigate the phenotypic consequences of reduced or abrogated SERT function.
- To compare the effects observed in mouse models with human genetic findings.
Main Methods:
- Utilizing mouse models with non-functional or impaired SERT.
- Analyzing phenotypic changes across behavioral, physiological, and metabolic domains.
- Correlating mouse findings with human genetic association studies.
Main Results:
- Mice with altered SERT function exhibited over 50 distinct phenotypes, including anxiety, gut dysfunction, bone weakness, and obesity with metabolic syndrome.
- These effects are influenced by gene-environment and gene-gene interactions.
- Human genetic variants impacting SERT function appear to produce phenotypes mirroring those in mice.
Conclusions:
- Reduced SERT function leads to a broad spectrum of health problems.
- Mouse models provide valuable insights into the complex phenotypes associated with SERT dysfunction.
- Human genetic variants affecting SERT show a parallel phenotypic landscape, underscoring the transporter's critical role.
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