ArticleJournal of central nervous system disease2014
Temporal- and Location-Specific Alterations of the GABA Recycling System in Mecp2 KO Mouse Brains.
Article in Journal of central nervous system disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Review
- Comprehensive Analysis of GABAInternational journal of molecular sciences · 2020Article
- Rescue of PB-resistant neonatal seizures with single-dose of small-molecule TrkB antagonist show long-term benefits.Epilepsy research · 2020Article
- Rett Syndrome and CDKL5 Deficiency Disorder: From Bench to Clinic.International journal of molecular sciences · 2019Review
- Rett syndrome (MECP2) and succinic semialdehyde dehydrogenase (ALDH5A1) deficiency in a developmentally delayed female.Molecular genetics & genomic medicine · 2019Article
- MeCP2 Deficiency in Neuroglia: New Progress in the Pathogenesis of Rett Syndrome.Frontiers in molecular neuroscience · 2017Review
- A Role for Diminished GABA Transporter Activity in the Cortical Discharge Phenotype of MeCP2-Deficient Mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
- Recent advances in understanding synaptic abnormalities in Rett syndrome.F1000Research · 2015Review
- Twenty-four hour quantitative-EEG and in-vivo glutamate biosensor detects activity and circadian rhythm dependent biomarkers of pathogenesis in Mecp2 null mice.Frontiers in systems neuroscience · 2014Article
- New insights into Rett syndrome pathogenesis: defining the role of MEPC2 in DNA damage.Frontiers in neurologyReview
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Rett syndrome (RTT), associated with mutations in methyl-CpG-binding protein 2 (Mecp2), is linked to diverse neurological symptoms such as seizures, motor disabilities, and cognitive impairments. An altered GABAergic system has been proposed as one of many underlying pathologies of progressive neurodegeneration in several RTT studies. This study for the first time investigated the temporal- and location-specific alterations in the expression of γ-amino butyric acid (GABA) transporter 1 (GAT-1), vesicular GABA transporter (vGAT), and glutamic acid decarboxylase 67kD (GAD67) in wild type (WT) and knockout (KO) mice in the Mecp2(tm1.1Bird/y) mouse model of RTT. Immunohistochemistry (IHC) co-labeling of GAT-1 with vGAT identified GABAergic synapses that were quantitated for mid-sagittal sections in the frontal cortex (FC), hippocampal dentate gyrus (DG), and striatum (Str). An age-dependent increase in the expression of synaptic GABA transporters, GAT-1, and vGAT, was observed in the FC and DG in WT brains. Mecp2 KO mice showed a significant alteration in this temporal profile that was location-specific, only in the FC. GAD67-positive cell densities also showed an age-dependent increase in the FC, but a decrease in the DG in WT mice. However, these densities were not significantly altered in the KO mice in the regions examined in this study. Therefore, the significant location-specific downregulation of synaptic GABA transporters in Mecp2 KO brains with unaltered densities of GAD67-positive interneurons may highlight the location-specific synaptic pathophysiology in this model of RTT.
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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.