ArticleThe Journal of physiology2015
Impaired CO2 sensitivity of astrocytes in a mouse model of Rett syndrome.
Article in The Journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Variable expression ofProceedings of the National Academy of Sciences of the United States of America · 2024Pooled it
- Review
- Carbogen Inhalation Therapy for Epileptic Seizures: Mechanisms, Evidence, and Future Directions.CNS neuroscience & therapeutics · 2025Review
- Kir4.1 channels contribute to astrocyte COCommunications biology · 2024Article
- Potential for New Therapeutic Approaches by Targeting Lactate and pH Mediated Epigenetic Dysregulation in Major Mental Diseases.Biomedicines · 2024Review
- Article
- Whole-brain analysis of CObioRxiv : the preprint server for biology · 2023Article
- Breathing disturbances in Rett syndrome.Handbook of clinical neurology · 2022Review
- Disordered breathing in a Pitt-Hopkins syndrome model involves Phox2b-expressing parafacial neurons and aberrant Nav1.8 expression.Nature communications · 2021Article
- Loss of MeCP2 increases GABA uptake by astrocytes to suppress tonic inhibition of CA1 pyramidal neurons.Journal of neurophysiology · 2021Article
- Anti-Semaphorin 4D Rescues Motor, Cognitive, and Respiratory Phenotypes in a Rett Syndrome Mouse Model.International journal of molecular sciences · 2021Article
- Role of Satb1 and Satb2 Transcription Factors in the Glutamate Receptors Expression and CaInternational journal of molecular sciences · 2021Article
- Analysis of Astroglial Secretomic Profile in the Mecp2-Deficient Male Mouse Model of Rett Syndrome.International journal of molecular sciences · 2021Article
- KGlia · 2021Article
- Epigenetics modifiers: potential hub for understanding and treating neurodevelopmental disorders from hypoxic injury.Journal of neurodevelopmental disorders · 2020Review
- The Pathophysiology of Rett Syndrome With a Focus on Breathing Dysfunctions.Physiology (Bethesda, Md.) · 2020Review
- Astrocytes Modulate Baroreflex Sensitivity at the Level of the Nucleus of the Solitary Tract.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Glial Dysfunction in MeCP2 Deficiency Models: Implications for Rett Syndrome.International journal of molecular sciences · 2019Review
- Reduced computational modelling of Kölliker-Fuse contributions to breathing patterns in Rett syndrome.The Journal of physiology · 2019Article
- The role of PHOX2B-derived astrocytes in chemosensory control of breathing and sleep homeostasis.The Journal of physiology · 2019Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Rett syndrome, a prototypical neurological disorder caused by loss of function of the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2) gene, is associated with a severely disordered breathing pattern and reduced ventilatory CO2 sensitivity. In a mouse model of Rett syndrome (MeCP2 knockout), re-introduction of the MeCP2 gene selectively in astrocytes rescues normal respiratory phenotype. In the present study we determined whether the metabolic and/or signalling functions of astrocytes are affected by testing the hypotheses that in conditions of MeCP2 deficiency, medullary astrocytes are unable to produce/release appropriate amounts of lactate or detect changes in PCO2/[H(+) ], or both. No differences in tonic or hypoxia-induced release of lactate from the ventral surface of the medulla oblongata or cerebral cortex in brain slices of MeCP2-knockout and wild-type mice were found. In brainstem slices of wild-type mice, respiratory acidosis triggered robust elevations in [Ca(2+) ]i in astrocytes residing near the ventral surface of the medulla oblongata. The magnitude of CO2 -induced [Ca(2+) ]i responses in medullary astrocytes was markedly reduced in conditions of MeCP2 deficiency, whereas [Ca(2+) ]i responses to ATP were unaffected. These data suggest that (i) metabolic function of astrocytes in releasing lactate into the extracellular space is not affected by MeCP2 deficiency, and (ii) MeCP2 deficiency impairs the ability of medullary astrocytes to sense changes in PCO2/[H(+) ]. Taken together with the evidence of severely blunted ventilatory sensitivity to CO2 in mice with conditional MeCP2 deletion in astroglia, these data support the hypothesis of an important role played by astrocytes in central respiratory CO2 /pH chemosensitivity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.