ArticlePloS one2021
Substantial acetylcholine reduction in multiple brain regions of Mecp2-deficient female rats and associated behavioral abnormalities.
Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Lac-Phe elicits anxiolytic-like effects associated with monoaminergic signaling in mice.Translational psychiatry · 2026Article
- Choline supplementation partially reverses prefrontal neurochemical deficits induced by perinatal opioid exposure.Scientific reports · 2026Article
- Mecp2 deficiency induces dysphagia in a preclinical model of Rett syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Reversal of neurological deficits by painless nerve growth factor in a mouse model of Rett syndrome.Brain : a journal of neurology · 2024Article
- Optimized Administration of the MACS chemical neuroscience · 2022Article
- Clinical and Preclinical Evidence for MNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- Excitation and Inhibition Imbalance in Rett Syndrome.Frontiers in neuroscience · 2022Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
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Abstract
Rett syndrome (RTT) is a neurodevelopmental disorder with X-linked dominant inheritance caused mainly by mutations in the methyl-CpG-binding protein 2 (MECP2) gene. The effects of various Mecp2 mutations have been extensively assessed in mouse models, but none adequately mimic the symptoms and pathological changes of RTT. In this study, we assessed the effects of Mecp2 gene deletion on female rats (Mecp2+/-) and found severe impairments in social behavior [at 8 weeks (w), 12 w, and 23 w of age], motor function [at 16 w and 26 w], and spatial cognition [at 29 w] as well as lower plasma insulin-like growth factor (but not brain-derived neurotrophic factor) and markedly reduced acetylcholine (30%-50%) in multiple brain regions compared to female Mecp2+/+ rats [at 29 w]. Alternatively, changes in brain monoamine levels were relatively small, in contrast to reports on mouse Mecp2 mutants. Female Mecp2-deficient rats express phenotypes resembling RTT and so may provide a robust model for future research on RTT pathobiology and treatment.
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