ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Exogenous brain-derived neurotrophic factor rescues synaptic dysfunction in Mecp2-null mice.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.
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Who cites it
102 citing papers in PubMed, 182 citations in OpenAlex.
- Neural peer pressure: intercellular dynamics and emergent phenotypes in the mosaic Rett syndrome brain.Cell communication and signaling : CCS · 2026Review
- MeCP2 regulates cell-type-specific functions of depressive-like symptoms in the nucleus accumbens.Experimental & molecular medicine · 2026Article
- Rett Syndrome: Thinking Beyond Brain Borders.Advances in experimental medicine and biology · 2025Review
- Lactobacillus-derived extracellular vesicles counteract Aβ42-induced abnormal transcriptional changes through the upregulation of MeCP2 and Sirt1 and improve Aβ pathology in Tg-APP/PS1 mice.Experimental & molecular medicine · 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
- iPSC toolbox for understanding and repairing disrupted brain circuits in autism.Molecular psychiatry · 2022Review
- Excitation and Inhibition Imbalance in Rett Syndrome.Frontiers in neuroscience · 2022Review
- Breathing Abnormalities During Sleep and Wakefulness in Rett Syndrome: Clinical Relevance and Paradoxical Relationship With Circulating Pro-oxidant Markers.Frontiers in neurology · 2022Article
- Breathing disturbances in Rett syndrome.Handbook of clinical neurology · 2022Review
- Article
- The role of astrocytes in the nucleus tractus solitarii in maintaining central control of autonomic function.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Review
- GABAergic System Dysfunction in Autism Spectrum Disorders.Frontiers in cell and developmental biology · 2021Review
- Restoration of motor learning in a mouse model of Rett syndrome following long-term treatment with a novel small-molecule activator of TrkB.Disease models & mechanisms · 2020Article
- The Pathophysiology of Rett Syndrome With a Focus on Breathing Dysfunctions.Physiology (Bethesda, Md.) · 2020Review
- The antitussive cloperastine improves breathing abnormalities in a Rett Syndrome mouse model by blocking presynaptic GIRK channels and enhancing GABA release.Neuropharmacology · 2020Article
- Development of the Autonomic Nervous System: Clinical Implications.Seminars in neurology · 2020Review
- Nuclear receptor corepressors in intellectual disability and autism.Molecular psychiatry · 2020Review
- An Increase of Excitatory-to-Inhibitory Synaptic Balance in the Contralateral Cortico-Striatal Pathway Underlies Improved Stroke Recovery in BDNF Val66Met SNP Mice.Neurorehabilitation and neural repair · 2019Article
- Article
- Autism Spectrum Disorder-Related Syndromes: Modeling withInternational journal of molecular sciences · 2019Review
42 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Postnatal deficits in brain-derived neurotrophic factor (BDNF) are thought to contribute to pathogenesis of Rett syndrome (RTT), a progressive neurodevelopmental disorder caused by mutations in the gene encoding methyl-CpG-binding protein 2 (MeCP2). In Mecp2-null mice, a model of RTT, BDNF deficits are most pronounced in structures important for autonomic and respiratory control, functions that are severely affected in RTT patients. However, relatively little is known about how these deficits affect neuronal function or how they may be linked to specific RTT endophenotypes. To approach these issues, we analyzed synaptic function in the brainstem nucleus tractus solitarius (nTS), the principal site for integration of primary visceral afferent inputs to central autonomic pathways and a region in which we found markedly reduced levels of BDNF in Mecp2 mutants. Our results demonstrate that the amplitude of spontaneous miniature and evoked EPSCs in nTS neurons is significantly increased in Mecp2-null mice and, accordingly, that mutant cells are more likely than wild- type cells to fire action potentials in response to primary afferent stimulation. These changes occur without any increase in intrinsic neuronal excitability and are unaffected by blockade of inhibitory GABA currents. However, this synaptopathy is associated with decreased BDNF availability in the primary afferent pathway and can be rescued by application of exogenous BDNF. On the basis of these findings, we hypothesize that altered sensory gating in nTS contributes to cardiorespiratory instability in RTT and that nTS is a site at which restoration of normal BDNF signaling could help reestablish normal homeostatic controls.
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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.