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Modulation of prefrontal cortex excitation/inhibition balance rescues social behavior in CNTNAP2 -deficient mice
Open accessAbstract
Using optogenetics to modulate the excitation/inhibition balance in the prefrontal cortex of an autism-like mouse model rescued social behavior deficits.
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In the citing paper
“while in CNTNAP2 deficient mice a decreased ratio of GABA to glutamate is seen in the medial prefrontal cortex (Selimbeyoglu et al. 2017), a finding paralleling results in autism patients (Harada et al. 2011).”
From Dysfunctional Autism Risk Genes Cause Circuit-Specific Connectivity Deficits With Distinct Developmental Trajectories (2018) · cites this paper as Selimbeyoglu et al. 2017
In the citing paper
“Although our experiment cannot prove a direct cause–effect relationship, we have shown a time-dependent relationship between the altered connectivity in prefrontal and ventral striatal networks that may be related to the imbalanced excitation/inhibition in mPFC of CNTNAP2−/− mice (Selimbeyoglu et al. 2017).”
From Dysfunctional Autism Risk Genes Cause Circuit-Specific Connectivity Deficits With Distinct Developmental Trajectories (2018) · cites this paper as Selimbeyoglu et al. 2017
In the citing paper
“social deficits present in mice lacking the Cntnap2 gene were rescued by correcting E/I imbalance via optogenetic activation of inhibitory PV neurons or inhibition of excitatory pyramidal neurons in the mPFC [126].”
From Neural circuits regulating prosocial behaviors (2023) · cites this paper as [126]
In the citing paper
“earlier findings that decreasing mPFC excitatory activity can rescue social deficits in an ASD mouse model24”
From Regulation of autism-relevant behaviors by cerebellar-prefrontal cortical circuits (2020) · cites this paper as [24]
In the citing paper
“Neural circuit manipulation in combination with neural recordings provide direct evidence that elevated mPFC activity results in ASD-related phenotypes, whereas decreasing mPFC activity is sufficient to rescue abnormal behaviors in ASD models22,23,24.”
From Regulation of autism-relevant behaviors by cerebellar-prefrontal cortical circuits (2020) · cites this paper as [24]
In the citing paper
“Consistent with these results, social deficits in the CNTNP2-deficient mouse model of autism could be rescued by modulating the excitability of pyramidal neurons (Selimbeyoglu et al., 2017).”
From Human Gut Microbiota from Autism Spectrum Disorder Promote Behavioral Symptoms in Mice (2019) · cites this paper as Selimbeyoglu et al., 2017
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Metadata
- Authors
- Selimbeyoglu, A., Kim, C. K., Inoue, M., Lee, S. Y., Hong, A. S. O., Kauvar, I., Ramakrishnan, C., Fenno, L. E., Davidson, T. J., Wright, M., & Deisseroth, K.
- Affiliations
- Stanford University (US)
- Stanford Medicine (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Deisseroth, Karl
- ORCID
- Venue
- Science Translational Medicine
- Published
- 2017-08-02
- Volume
- 9
- Issue
- 401
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC5723386
- OpenAlex
- W2740920123
- Cited by
- 326
- References
- 47
- Citations by year
- 2026: 30 · 2025: 40 · 2024: 34 · 2023: 35 · 2022: 37 · 2021: 45 · 2020: 41 · 2019: 38 · 2018: 24 · 2017: 2
- FWCI
- 19.06
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute (award299942, None)
- 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
- CNTNAP2, prefrontal cortex, excitation-inhibition balance, social behavior, autism spectrum disorder, knockout mice, neural circuit modulation, social dysfunction
- MeSH terms
- Animals, Autistic Disorder, Behavior, Animal, Genetic Engineering, Membrane Proteins, Mice, Inbred C57BL, Movement, Nerve Tissue Proteins, Neurons, Parvalbumins, Social Behavior, Prefrontal Cortex, Mice, Knockout, Opsins
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