ArticleJournal of neurophysiology2011
Selective impact of MeCP2 and associated histone deacetylases on the dynamics of evoked excitatory neurotransmission.
Article in Journal of neurophysiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Neurophysiology of acute and chronic pain: from genes to pain symptoms.BJA education · 2025Review
- Zebrafish mecp2 null-mutation increases anxiety and cortisol levels but no change in adult social preference and larval chemically-induced hyperlocomotion.BMC neuroscience · 2025Article
- MeCP2 prevents against sustained ketamine-induced synaptic depression at inhibitory synapses.iScience · 2025Article
- MeCP2 loss-of-function dysregulates microRNAs regionally and disrupts excitatory/inhibitory synaptic transmission balance.Hippocampus · 2022Article
- Excitation and Inhibition Imbalance in Rett Syndrome.Frontiers in neuroscience · 2022Review
- Rett Syndrome andNeuropsychiatric disease and treatment · 2022Review
- The Role of MicroRNAs in Cerebellar Development and Autism Spectrum Disorder During Embryogenesis.Molecular neurobiology · 2017Review
- Excitatory synapses are stronger in the hippocampus of Rett syndrome mice due to altered synaptic trafficking of AMPA-type glutamate receptors.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Excitation/inhibition imbalance and impaired synaptic inhibition in hippocampal area CA3 of Mecp2 knockout mice.Hippocampus · 2015Article
- GABAA receptor antagonism ameliorates behavioral and synaptic impairments associated with MeCP2 overexpression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014Article
- Transcriptional co-repressors and memory storage.Neuropharmacology · 2014Review
- GABA and glutamate pathways are spatially and developmentally affected in the brain of Mecp2-deficient mice.PloS one · 2014Article
- Breathing challenges in Rett syndrome: lessons learned from humans and animal models.Respiratory physiology & neurobiology · 2013Review
- Epigenetics of Alzheimer's disease and frontotemporal dementia.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2013Review
- Article
- Histone acetylation: molecular mnemonics on the chromatin.Nature reviews. Neuroscience · 2013Review
- The impact of MeCP2 loss- or gain-of-function on synaptic plasticity.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2013Review
- Article
- 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.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- A mouse model for MeCP2 duplication syndrome: MeCP2 overexpression impairs learning and memory and synaptic transmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
An imbalance between the strengths of excitatory and inhibitory synaptic inputs has been proposed as the cellular basis of autism and related neurodevelopmental disorders. Previous studies examining spontaneous levels of excitatory and inhibitory neurotransmission in the forebrain regions of methyl-CpG-binding protein 2 (Mecp2) mutant mice, models of the autism spectrum disorder Rett syndrome, have identified a decrease in excitatory drive, in some cases coupled with an increase in inhibitory synaptic strength, as a major source of this imbalance. Here, we reevaluated this question by examining the short-term dynamics of evoked neurotransmission between hippocampal neurons cultured from MeCP2 knockout mice and found a marked increase in evoked excitatory neurotransmission that is consistent with an increase in presynaptic release probability. This increase in evoked excitatory drive was not matched with alterations in evoked inhibitory neurotransmission. Moreover, we observed similar excitatory drive specific changes after the loss of key histone deacetylases (histone deacetylase 1 and 2) that form a complex with MeCP2 and mediate transcriptional regulation. These findings suggest a distinct role for MeCP2 and its cofactors in the regulation of evoked excitatory neurotransmission compared with their essential role in basal synaptic activity.
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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.