Activation of the Medial Prefrontal Cortex Reverses Cognitive and Respiratory Symptoms in a Mouse Model of Rett Syndrome
Open accessAbstract
Rett syndrome (RTT) is a severe neurodevelopmental disorder caused by loss-of-function mutations in the gene encoding methyl-CpG-binding protein 2 (MeCP2; Amir et al., 1999), a transcriptional regulatory protein (Klose et al., 2005). Mouse models of RTT (Mecp2 mutants) exhibit excitatory hypoconnectivity in the medial prefrontal cortex (mPFC; Sceniak et al., 2015), a region critical for functions that are abnormal in RTT patients, ranging from learning and memory to regulation of visceral homeostasis (Riga et al., 2014). The present study was designed to test the hypothesis that increasing the activity of mPFC pyramidal neurons in heterozygous female Mecp2 mutants (Hets) would ameliorate RTT-like symptoms, including deficits in respiratory control and long-term retrieval of auditory conditioned fear. Selective activation of mPFC pyramidal neurons in adult animals was achieved by bilateral infection with an AAV8 vector expressing excitatory hm3D(Gq) DREADD (Designer Receptors Exclusively Activated by Designer Drugs) (Armbruster et al., 2007) under the control of the CamKIIa promoter. DREADD activation in Mecp2 Hets completely restored long-term retrieval of auditory conditioned fear, eliminated respiratory apneas, and reduced respiratory frequency variability to wild-type (Wt) levels. Reversal of respiratory symptoms following mPFC activation was associated with normalization of Fos protein levels, a marker of neuronal activity, in a subset of brainstem respiratory neurons. Thus, despite reduced levels of MeCP2 and severe neurological deficits, mPFC circuits in Het mice are sufficiently intact to generate normal behavioral output when pyramidal cell activity is increased. These findings highlight the contribution of mPFC hypofunction to the pathophysiology of RTT and raise the possibility that selective activation of cortical regions such as the mPFC could provide therapeutic benefit to RTT patients.
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Restoring Mecp2 levels within the PFC in mice via CRISPR-Cas9 or DREADDS can restore some endophenotypes such as social recognition deficits or long-term retrieval of auditory conditioned fear.
“Restoring Mecp2 levels within the PFC in mice via state-of-the-art techniques such as CRISPR-Cas9 or DREADDS can restore some of the endophenotypes such as social recognition deficits or long-term retrieval of auditory conditioned fear [267, 270, 271].”
From Development of prefrontal cortex (2022) · cites this paper as [267]
The Results section reports that DREADD activation of medial prefrontal cortex neurons restored long-term retrieval of auditory conditioned fear in Mecp2-mutant mice 24 hours after training. The intervention activated neurons; the paper does not report restoring Mecp2 levels, using CRISPR-Cas9, or rescuing social recognition deficits. Page numbers are unavailable in our copy. (LLM, conf=0.90)
Experimental — accuracy not yet measuredIn Rett syndrome, a severe NDD with specific cognitive and behavioral features, there is a strong PFC hypofunction with structural abnormalities.
“In Rett syndrome, a severe NDD with specific cognitive and behavioral features, there is a strong PFC hypofunction with structural abnormalities [267–269].”
From Development of prefrontal cortex (2022) · cites this paper as [267]
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- Authors
- Howell, C. J., Sceniak, M. P., Lang, M., Krakowiecki, W., Abouelsoud, F. E., Lad, S. U., Yu, H., & Katz, D. M.
- Affiliations
- Case Western Reserve University (US)
- Corresponding author
- Katz, David M.
- Venue
- eneuro
- Publisher
- Society for Neuroscience
- Published
- 2017-11
- Volume
- 4
- Issue
- 6
- Pages
- ENEURO.0277-17.2017
- ISSN
- 2373-2822 (ISSN-L)
- PMC
- PMC5762598
- OpenAlex
- W2776221434
- Cited by
- 23
- References
- 64
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- FWCI
- 1.63
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- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- eNeuro (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- HHS | National Institutes of Health (NS057398, NS098574-02)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroscience of respiration and sleep
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- Rett syndrome, MeCP2, medial prefrontal cortex, DREADD, respiratory control, Fos expression, brainstem respiratory neurons, neurodevelopmental disorders, gene therapy
- MeSH terms
- Animals, Auditory Perception, Cognition, Conditioning, Psychological, Disease Models, Animal, Fear, Female, Genetic Vectors, Mice, Inbred BALB C, Mice, Transgenic, Random Allocation, Receptors, Cell Surface, Respiration, Designer Drugs, Rett Syndrome, Prefrontal Cortex, Pyramidal Cells, Methyl-CpG-Binding Protein 2, Mice, 129 Strain
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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