Early alterations in a mouse model of Rett syndrome: the GABA developmental shift is abolished at birth.
Animals
Bumetanide
/ pharmacology
Methyl-CpG-Binding Protein 2
/ physiology
Mice
Mice, Inbred C57BL
Mice, Knockout
Neuronal Plasticity
Neurons
/ drug effects
Receptors, GABA-A
/ metabolism
Respiratory System
/ drug effects
Rett Syndrome
/ drug therapy
Sodium Potassium Chloride Symporter Inhibitors
/ pharmacology
Synaptic Potentials
Synaptic Transmission
/ drug effects
gamma-Aminobutyric Acid
/ metabolism
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
25 06 2019
25 06 2019
Historique:
received:
14
02
2019
accepted:
11
06
2019
entrez:
27
6
2019
pubmed:
27
6
2019
medline:
28
10
2020
Statut:
epublish
Résumé
Genetic mutations of the Methyl-CpG-binding protein-2 (MECP2) gene underlie Rett syndrome (RTT). Developmental processes are often considered to be irrelevant in RTT pathogenesis but neuronal activity at birth has not been recorded. We report that the GABA developmental shift at birth is abolished in CA3 pyramidal neurons of Mecp2
Identifiants
pubmed: 31239460
doi: 10.1038/s41598-019-45635-9
pii: 10.1038/s41598-019-45635-9
pmc: PMC6592949
doi:
Substances chimiques
Mecp2 protein, mouse
0
Methyl-CpG-Binding Protein 2
0
Receptors, GABA-A
0
Sodium Potassium Chloride Symporter Inhibitors
0
Bumetanide
0Y2S3XUQ5H
gamma-Aminobutyric Acid
56-12-2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
9276Références
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