R-Baclofen reverses cognitive deficits and improves social interactions in two lines of 16p11.2 deletion mice
Open accessAbstract
Human chromosome 16p11.2 microdeletion is among the most common gene copy number variations (CNVs) known to confer risk for intellectual disability (ID) and autism spectrum disorder (ASD) and affects an estimated 3 in 10 000 people. Caused by a single copy deletion of ~27 genes, 16p11.2 microdeletion syndrome is characterized by ID, impaired language, communication and socialization skills, and ASD. Studies in animal models where a single copy of the syntenic 16p11.2 region has been deleted have revealed morphological, behavioral, and electrophysiological abnormalities. Previous studies suggested the possibility of some overlap in the mechanisms of pathophysiology in 16p11.2 microdeletion syndrome and fragile X syndrome. Improvements in fragile X phenotypes have been observed following chronic treatment with R -baclofen, a selective agonist of GABA B receptors. We were therefore motivated to investigate the effects of chronic oral R -baclofen administration in two independently generated mouse models of 16p11.2 microdeletion syndrome. In studies performed across two independent laboratories, we found that chronic activation of GABA B receptors improved performance on a series of cognitive and social tasks known to be impaired in two different 16p11.2 deletion mouse models. Our findings suggest that R -baclofen may have clinical utility for some of the core symptoms of human 16p11.2 microdeletion syndrome.
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All three lines of 16p11.2+/− mice display social deficits in various testing paradigms and an array of cognitive deficits.
“All 3 lines of 16p11.2+/− mice display social deficits in various testing paradigms [59–64], and an array of cognitive deficits [4, 59, 62–68].”
From 16p11.2 Copy Number Variations and Neurodevelopmental Disorders (2020) · cites this paper as [64]
Hyperlocomotion is broadly reported in 16p11.2+/− mice, another behavioral feature that does not coincide directly with human symptomology.
“Hyperlocomotion is also broadly reported in 16p11.2+/− mice [4, 5, 59, 61, 63, 64, 70], another behavioral feature that does not coincide directly with human symptomology.”
From 16p11.2 Copy Number Variations and Neurodevelopmental Disorders (2020) · cites this paper as [64]
R-baclofen improves performance of 16p11.2 hemideletion mice on several cognitive tasks.
“R-baclofen improves performance of 16p11.2+/− mice in several cognitive tasks, while hyperlocomotion and USVs are unaffected [64].”
From 16p11.2 Copy Number Variations and Neurodevelopmental Disorders (2020) · cites this paper as [64]
R-baclofen does not alter hyperlocomotion or ultrasonic vocalizations in 16p11.2 hemideletion mice.
“R-baclofen improves performance of 16p11.2+/− mice in several cognitive tasks, while hyperlocomotion and USVs are unaffected [64].”
From 16p11.2 Copy Number Variations and Neurodevelopmental Disorders (2020) · cites this paper as [64]
R-baclofen has therapeutic efficacy in Fmr1-deficient mice that share a similar synaptic plasticity phenotype.
“as R-baclofen displayed therapeutic efficacy in Fmr1-deficient mice with a similar synaptic plasticity phenotype [64]”
From 16p11.2 Copy Number Variations and Neurodevelopmental Disorders (2020) · cites this paper as [64]
Systemic administration of R-Baclofen, a GABA B receptor agonist, reversed the social deficits present in two different 16p11.2 deletion mouse models.
“systemic administration of R-Baclofen, a GABA B receptor agonist, reversed the social deficits present in two different 16p11.2deletion mouse models [130].”
From Neural circuits regulating prosocial behaviors (2023) · cites this paper as [130]
Arbaclofen has rescued behavioral deficits including social deficits in mouse models of idiopathic ASD, deletion of 16p11.2, and FXS.
“For many subtypes of ASD, there is a GABAB deficit and arbaclofen has rescued the behavioral deficits including social deficits in the mouse models of idiopathic ASD [127], deletion of 16p11.2 [128], and FXS [129].”
From An Update on Psychopharmacological Treatment of Autism Spectrum Disorder (2022) · cites this paper as [128]
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- Authors
- Stoppel, L. J., Kazdoba, T. M., Schaffler, M. D., Preza, A. R., Heynen, A., Crawley, J. N., & Bear, M. F.
- Affiliations
- Massachusetts Institute of Technology (US)
- University of California Davis Medical Center (US)
- Corresponding author
- Bear, Mark F
- Venue
- Neuropsychopharmacology
- Published
- 2017-10-06
- Volume
- 43
- Issue
- 3
- Pages
- 513-524
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- PMC
- PMC5770771
- OpenAlex
- W2763013404
- Cited by
- 92
- References
- 51
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 11 · 2023: 15 · 2022: 12 · 2021: 13 · 2020: 11 · 2019: 15 · 2018: 5
- FWCI
- 5.63
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Neuropsychopharmacology (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by-nc-sa)
- eScholarship (California Digital Library) (submittedVersion, cc-by-nc-sa)
- Funders
- Simons Foundation
- Amgen
- Simons Foundation Autism Research Initiative
- National Institute of Mental Health (R01MH106469, T32MH074249, T32MH073124)
- National Institute of Neurological Disorders and Stroke (R01NS085709)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (U54HD079125)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genomic variations and chromosomal abnormalities
- Life Sciences › Neuroscience › Developmental Neuroscience › Williams Syndrome Research
- Keywords
- R-baclofen, GABA-B receptor agonist, cognitive impairment, social interaction deficits, autism spectrum disorder, intellectual disability, fragile X syndrome, gene copy number variation, mouse model, chronic drug administration
- MeSH terms
- Animals, Autistic Disorder, Baclofen, Chromosome Deletion, Chromosomes, Human, Pair 16, Cognition Disorders, Disease Models, Animal, Female, Learning Disabilities, Male, Memory Disorders, Intellectual Disability, Mice, Inbred C57BL, Psychotropic Drugs, Social Behavior, Species Specificity, Chromosome Disorders, Mice, 129 Strain, GABA-B Receptor Agonists
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