ArticleExperimental physiology2013
Increasing brain serotonin corrects CO2 chemosensitivity in methyl-CpG-binding protein 2 (Mecp2)-deficient mice.
Article in Experimental physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 45 citations in OpenAlex.
- Carotid body dysfunction contributes to respiratory instability in Rett syndrome.Current biology : CB · 2026Article
- MeCP2 at the crossroads of hypoxia, oxidative stress, and gene regulation in Rett syndrome.Epigenomics · 2025Review
- Retrotrapezoid nucleus chemoreception: mechanisms of function and contributions to disordered breathing in disease.Trends in neurosciences · 2025Review
- Sleep Disorders in Children with Rett Syndrome.Children (Basel, Switzerland) · 2025Review
- An automated respiratory data pipeline for waveform characteristic analysis.The Journal of physiology · 2023Article
- A narrative review of the mechanisms and consequences of intermittent hypoxia and the role of advanced analytic techniques in pediatric autonomic disorders.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2023Review
- Advancing respiratory-cardiovascular physiology with the working heart-brainstem preparation over 25 years.The Journal of physiology · 2022Review
- Molecular Signatures of Response to Mecasermin in Children With Rett Syndrome.Frontiers in neuroscience · 2022Article
- Breathing disturbances in Rett syndrome.Handbook of clinical neurology · 2022Review
- Fluoxetine increases brain MeCP2 immuno-positive cells in a female Mecp2 heterozygous mouse model of Rett syndrome through endogenous serotonin.Scientific reports · 2021Article
- The Pathophysiology of Rett Syndrome With a Focus on Breathing Dysfunctions.Physiology (Bethesda, Md.) · 2020Review
- Drug Studies on Rett Syndrome: From Bench to Bedside.Journal of autism and developmental disorders · 2020Review
- Treating Rett syndrome: from mouse models to human therapies.Mammalian genome : official journal of the International Mammalian Genome Society · 2019Review
- Reduced computational modelling of Kölliker-Fuse contributions to breathing patterns in Rett syndrome.The Journal of physiology · 2019Article
- The Kölliker-Fuse nucleus orchestrates the timing of expiratory abdominal nerve bursting.Journal of neurophysiology · 2018Article
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- Deficiency of GABAergic synaptic inhibition in the Kölliker-Fuse area underlies respiratory dysrhythmia in a mouse model of Rett syndrome.The Journal of physiology · 2016Article
- Breathing abnormalities in a female mouse model of Rett syndrome.The journal of physiological sciences : JPS · 2015Article
- Impaired CO2 sensitivity of astrocytes in a mouse model of Rett syndrome.The Journal of physiology · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Mice deficient in the transcription factor methyl-CpG-binding protein 2 (Mecp2), a mouse model of Rett syndrome, display reduced CO2 chemosensitivity, which may contribute to their breathing abnormalities. In addition, patients with Rett syndrome and male mice that are null for Mecp2 show reduced levels of brain serotonin (5-HT). Serotonin is known to play a role in central chemosensitivity, and we hypothesized that increasing the availability of 5-HT in this mouse model would improve their respiratory response to CO2. Here we determined the apnoeic threshold in heterozygous Mecp2-deficient female mice and examined the effects of blocking 5-HT reuptake on the CO2 response in Mecp2-null male mice. Studies were performed in B6.129P2(C)-Mecp2(τm1.1Bird) null males and heterozygous females. In an in situ preparation, seven of eight Mecp2-deficient heterozygous females showed arrest of phrenic nerve activity when arterial CO2 was lowered to 3%, whereas the wild-types maintained phrenic nerve amplitude at 53 ± 3% of maximal. In vivo plethysmography studies were used to determine CO2 chemosensitivity in null males. These mice were exposed sequentially to 1, 3 and 5% CO2. The percentage increase in minute ventilation in response to increased inspired CO2 was less in Mecp2(-/y) than in Mecp2(+/y) mice. Pretreatment with citalopram, a selective 5-HT reuptake inhibitor (2.5 mg kg(-1) i.p.), 40 min prior to CO2 exposure, in Mecp2(-/y) mice resulted in an improvement in CO2 chemosensitivity to wild-type levels. These results suggest that decreased 5-HT in Mecp2-deficient mice reduces CO2 chemosensitivity, and restoring 5-HT levels can reverse this effect.
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