Chronic administration of AFQ056/Mavoglurant restores social behaviour in Fmr1 knockout mice
Abstract
Fragile X syndrome is caused by lack of FMR1 protein (FMRP) leading to severe symptoms, including intellectual disability, hyperactivity and autistic-like behaviour. FMRP is an RNA binding protein involved in the regulation of translation of specific target mRNAs upon stimulation of metabotropic glutamate receptor 5 (mGluR5) at the synapse. The absence of FMRP leads to enhanced activity of mGluR5 signal transduction pathways. Many conflicting results have been reported regarding social behaviour deficits in Fmr1 knockout mice, and little is known about the involvement of mGluR5 pathways on social behaviour. In this study, a three-chambered task was used to determine sociability and preference for social novelty in Fmr1 knockout mice. Disruption of Fmr1 functioning resulted in enhanced interaction with stranger mouse during sociability while no significant changes were observed during preference for social novelty assay. Chronic administration of a specific mGluR5 antagonist, AFQ056/Mavoglurant, was able to restore sociability behaviour of Fmr1 knockout mice to levels of wild type littermates. These results support the importance of mGluR5 signalling pathways on social interaction behaviour and that AFQ056/Mavoglurant might be useful as potential therapeutic intervention to rescue various behavioural aspects of the fragile X phenotype.
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Pharmacological mGluR5 antagonists rescue protein synthesis and many classic outcome measures in mouse and fly FXS models.
“have demonstrated that dampening mGluR5 signalling rescues protein synthesis and many of the classic outcome measures (TABLE 1) used in the mouse and fly models30–35.”
From Drug development for neurodevelopmental disorders: lessons learned from fragile X syndrome (2018) · cites this paper as [30]
Rescue of these behavioural phenotypes has been difficult to consolidate and to use as a guide for clinical studies.
“As a result, the rescue of these behavioural phenotypes has been difficult to consolidate and to use as a guide for clinical studies30,49,56,64,65.”
From Drug development for neurodevelopmental disorders: lessons learned from fragile X syndrome (2018) · cites this paper as [30]
Many classic behavioural phenotypes used as preclinical outcome measures are inconsistently observed in Fmr1-knockout mice.
“many of the other classic behavioural phenotypes used as outcome measures in preclinical studies are inconsistently observed in Fmr1-KO mice (such as open field, rotarod, elevated plus-maze, marble burying, self-grooming and most social paradigms).”
From Drug development for neurodevelopmental disorders: lessons learned from fragile X syndrome (2018) · cites this paper as [30]
In Fmr1-knockout mice, mGluR antagonists, GABAB agonists, and gene reinstatement beginning in young adult or adult mice can fully correct most behavioural, physiological, biochemical, and neuroanatomical alterations.
“treatment with mGluR antagonists (mavoglurant) and GABAB agonists (arbaclofen), as well as gene reinstatement in Fmr1-KO mice starting in young adult or adult mice, can fully correct most behavioural, physiological, biochemical and neuroanatomical alterations30,32,37.”
From Drug development for neurodevelopmental disorders: lessons learned from fragile X syndrome (2018) · cites this paper as [30]
Treatment with an mGluR5 antagonist in young adult or fully adult mice produced comprehensive correction of Fmr1-knockout phenotypes.
“Moreover, a comprehensive correction of Fmr1-KO phenotypes was achieved with mGluR5 antagonist treatment of young adult or fully adult mice30,32.”
From Drug development for neurodevelopmental disorders: lessons learned from fragile X syndrome (2018) · cites this paper as [30]
No human data are available for spinocerebellar ataxia type 1 because no suitable drug for clinical trials exists.
“No human data are available for SCA1 in the absence of a drug suitable for clinical trials30,32,37.”
From Drug development for neurodevelopmental disorders: lessons learned from fragile X syndrome (2018) · cites this paper as [30]
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- Authors
- Gantois, I., Pop, A. S., de Esch, C. E. F., Buijsen, R. A. M., Pooters, T., Gomez-Mancilla, B., Gasparini, F., Oostra, B. A., D’Hooge, R., & Willemsen, R.
- Affiliations
- KU Leuven (BE)
- Erasmus MC (NL)
- Novartis (Switzerland) (CH)
- Corresponding author
- Gantois, Ilse
- Venue
- Behavioural Brain Research
- Publisher
- Elsevier BV
- Published
- 2013-02
- Volume
- 239
- Pages
- 72-79
- ISSN
- 0166-4328 (ISSN-L)
- OpenAlex
- W1997037252
- Cited by
- 100
- References
- 59
- Citations by year
- 2025: 2 · 2024: 3 · 2023: 4 · 2022: 2 · 2021: 7 · 2020: 6 · 2019: 8 · 2018: 6 · 2017: 20 · 2016: 7 · 2015: 15 · 2014: 10 · 2013: 10
- FWCI
- 6.72
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Behavioural Brain Research (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- The Novartis Repository (Novartis) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Keywords
- fragile X syndrome, FMRP, Fmr1 knockout mice, mGluR5, metabotropic glutamate receptor 5, mGluR5 antagonist, social behavior, sociability, social novelty preference, autism-like behavior, translational therapy
- MeSH terms
- Animals, Disease Models, Animal, Fragile X Syndrome, Indoles, Male, Mice, Inbred C57BL, Social Behavior, Time Factors, Receptors, Metabotropic Glutamate, Mice, Knockout, Excitatory Amino Acid Antagonists, Mice, Fragile X Messenger Ribonucleoprotein 1, Receptor, Metabotropic Glutamate 5
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