Brain Activity Mapping in Mecp2 Mutant Mice Reveals Functional Deficits in Forebrain Circuits, Including Key Nodes in the Default Mode Network, that are Reversed with Ketamine Treatment
Open accessAbstract
Excitatory-inhibitory imbalance has been identified within specific brain microcircuits in models of Rett syndrome (RTT) and other autism spectrum disorders (ASDs). However, macrocircuit dysfunction across the RTT brain as a whole has not been defined. To approach this issue, we mapped expression of the activity-dependent, immediate-early gene product Fos in the brains of wild-type (Wt) and methyl-CpG-binding protein 2 ( Mecp2 )-null (Null) mice, a model of RTT, before and after the appearance of overt symptoms (3 and 6 weeks of age, respectively). At 6 weeks, Null mice exhibit significantly less Fos labeling than Wt in limbic cortices and subcortical structures, including key nodes in the default mode network. In contrast, Null mice exhibit significantly more Fos labeling than Wt in the hindbrain, most notably in cardiorespiratory regions of the nucleus tractus solitarius (nTS). Using nTS as a model, whole-cell recordings demonstrated that increased Fos expression in Nulls at 6 weeks of age is associated with synaptic hyperexcitability, including increased frequency of spontaneous and miniature EPSCs and increased amplitude of evoked EPSCs in Nulls. No such effect of genotype on Fos or synaptic function was seen at 3 weeks. In the mutant forebrain, reduced Fos expression, as well as abnormal sensorimotor function, were reversed by the NMDA receptor antagonist ketamine. In light of recent findings that the default mode network is hypoactive in autism, our data raise the possibility that hypofunction within this meta-circuit is a shared feature of RTT and other ASDs and is reversible.
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Ketamine treatment normalizes cortical activity in both young adults and adult mice.
“Ketamine treatment normalizes cortical activity in both young adults and adult mice 131,132 ,”
From Developmental timing and critical windows for the treatment of psychiatric disorders (2016) · cites this paper as [132]
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- Authors
- Kron, M., Howell, C. J., Adams, I. T., Ransbottom, M., Christian, D., Ogier, M., & Katz, D. M.
- Affiliations
- Case Western Reserve University (US)
- ORCID
- Katz, David M.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2012-10-03
- Volume
- 32
- Issue
- 40
- Pages
- 13860-13872
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3500840
- OpenAlex
- W2009942054
- Cited by
- 154
- References
- 11
- Citations by year
- 2026: 6 · 2025: 11 · 2024: 6 · 2023: 8 · 2022: 14 · 2021: 11 · 2020: 9 · 2019: 15 · 2018: 10 · 2017: 12 · 2016: 15 · 2015: 13 · 2014: 7 · 2013: 15 · 2012: 2
- FWCI
- 7.13
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- Funders
- Autism Speaks
- International Rett Syndrome Foundation
- National Institute of Neurological Disorders and Stroke (R01NS057398)
- 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
- Rett syndrome, default mode network, Fos expression, ketamine, excitatory-inhibitory imbalance, nucleus tractus solitarius, autism spectrum disorder, limbic cortex, NMDA receptor antagonists, sensorimotor function
- MeSH terms
- Animals, Autonomic Nervous System, Cerebellum, Disease Models, Animal, Female, Humans, Ketamine, Male, Nerve Net, Nerve Tissue Proteins, Synaptic Transmission, Organ Specificity, Rett Syndrome, Prosencephalon, Proto-Oncogene Proteins c-fos, Genes, fos, Solitary Nucleus, Mice, Knockout, Patch-Clamp Techniques, Gene Expression Regulation, Developmental, Excitatory Amino Acid Antagonists, Mice, Methyl-CpG-Binding Protein 2, Sensory Gating, Miniature Postsynaptic Potentials
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