ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2014
GABAA receptor antagonism ameliorates behavioral and synaptic impairments associated with MeCP2 overexpression.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
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- Increased Reliability of Visually-Evoked Activity in Area V1 of the MECP2-Duplication Mouse Model of Autism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Exploration of group II metabotropic glutamate receptor modulation in mouse models of Rett syndrome and MECP2 Duplication syndrome.Neuropharmacology · 2022Article
- Rett Syndrome andNeuropsychiatric disease and treatment · 2022Review
- TGF-β/Smad3 Signalling Modulates GABA Neurotransmission: Implications in Parkinson's Disease.International journal of molecular sciences · 2020Review
- Contextual Fear Extinction Induces Hippocampal Metaplasticity Mediated by Metabotropic Glutamate Receptor 5.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
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- Genetic studies in intellectual disability and related disorders.Nature reviews. Genetics · 2016Review
- Rescue of Methyl-CpG Binding Protein 2 Dysfunction-induced Defects in Newborn Neurons by Pentobarbital.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015Article
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Methyl-CpG-binding protein 2 (MeCP2) is a ubiquitously expressed transcriptional regulator with functional importance in the central nervous system. Loss-of-function mutations in MECP2 results in the neurodevelopmental disorder, Rett syndrome, whereas increased expression levels are associated with the neurological disorder, MECP2 duplication syndrome. Previous characterization of a mouse line overexpressing Mecp2 demonstrated that this model recapitulated key behavioral features of MECP2 duplication syndrome with specific deficits in synaptic plasticity and neurotransmission. Alterations in excitation/inhibition balance have been suggested to underlie neurodevelopmental disorders with recent data suggesting that picrotoxin (PTX), a GABAA receptor antagonist, rescues certain behavioral and synaptic phenotypes in a mouse model of Down syndrome. We therefore examined whether a similar treatment regimen would impact the behavioral and synaptic phenotypes in a mouse model of MECP2 duplication syndrome. We report that chronic treatment with low doses of PTX ameliorates specific behavioral phenotypes, including motor coordination, episodic memory impairments, and synaptic plasticity deficits. These findings suggest that GABAA receptor antagonists may offer a possible therapeutic target for the treatment of MECP2 duplication syndrome.
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