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Lipopolysaccharide-induced sickness behavior is not altered in male Fmr1-deficient mice
Danielle Santana-Coelho1, Samantha L Hodges2,3, Saul I Quintero1
1Department of Psychology and Neuroscience, Baylor University, Waco, Texas, USA.
Objectives:
Fragile X syndrome is the main monogenetic cause of intellectual disability and autism. Alterations in the immune system are commonly found in these developmental disorders. We and others have demonstrated that Fmr1 mutant mice present an altered response to immune stimuli. However, whether this altered immune response can influence the Fmr1 mutant behavioral outcomes in response to inflammation has not been fully investigated.
Materials And Methods:
In the current study, we examine the behavioral sickness response of male wildtype and knockout mice to the innate immune stimulus lipopolysaccharide (LPS) (0.1 mg/kg) to determine if Fmr1 mutants have altered sickness behavior. We used an enzyme-linked immunosorbent assay (ELISA) to measure changes in the cytokine interleukin-6 (IL-6) to determine that inflammation was induced in the mice. Sickness behavior was assessed in a wheel-running paradigm, and a tail suspension test was used to assess the depressive-like phenotype that follows sickness behavior in response to LPS.
Results:
The ELISA using blood serum confirmed a significant increase in IL-6 in mice that were treated with LPS. Treated Fmr1 mutants exhibited decreased distance traveled in the wheel running after LPS administration, similar to treated controls. Another cohort of animals treated with LPS were tested in the tail suspension test and exhibited no alterations in immobility time in response to LPS.
Conclusion:
Together, our data suggest that Fmr1 mutant mice do not have altered sickness behavior in response to a low dose of LPS.
Insights
Fragile X syndrome (FXS) mouse models show normal sickness behavior when exposed to lipopolysaccharide (LPS). This indicates that FXS does not alter behavioral responses to innate immune system activation.
Area of Science:
- Neuroscience
- Immunology
- Genetics
Background:
- Fragile X syndrome (FXS) is a leading genetic cause of intellectual disability and autism.
- Immune system dysregulation is frequently observed in FXS.
- Previous studies show altered immune responses in Fmr1 mutant mice, but their behavioral impact during inflammation is unclear.
Purpose of the Study:
- To investigate the sickness behavior of Fmr1 mutant mice in response to lipopolysaccharide (LPS).
- To determine if Fmr1 mutation affects behavioral outcomes during innate immune stimulation.
Main Methods:
- Male wildtype and Fmr1 knockout mice were administered LPS (0.1 mg/kg).
- Interleukin-6 (IL-6) levels were measured via ELISA to confirm inflammation.
- Sickness behavior was assessed using wheel-running activity.
- Depressive-like behavior was evaluated using the tail suspension test.
Main Results:
- LPS administration significantly increased IL-6 levels in both wildtype and Fmr1 mutant mice.
- Fmr1 mutants showed reduced wheel-running distance post-LPS, similar to controls.
- No significant alterations in immobility time were observed in the tail suspension test after LPS treatment.
Conclusions:
- Fmr1 mutant mice do not exhibit altered sickness behavior in response to low-dose LPS.
- The study suggests that Fmr1 mutation does not impact behavioral responses to acute innate immune challenge.
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