Abstract:
: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-/y mice and the glutamatergic/GABAergic postsynaptic currents (PSCs) ratio is increased. Two weeks later, GABA exerts strong excitatory actions, the glutamatergic/GABAergic PSCs ratio is enhanced, hyper-synchronized activity is present and metabotropic long-term depression (LTD) is impacted. One day before delivery, maternal administration of the NKCC1 chloride importer antagonist bumetanide restored these parameters but not respiratory or weight deficits, nor the onset of mortality. Results suggest that birth is a critical period in RTT with important alterations that can be attenuated by bumetanide raising the possibility of early treatment of the disorder.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Lozovaya N,Nardou R,Tyzio R,Chiesa M,Pons-Bennaceur A,Eftekhari S,Bui TT,Billon-Grand M,Rasero J,Bonifazi P,Guimond D,Gaiarsa JL,Ferrari DC,Ben-Ari Ydoi
10.1038/s41598-019-45635-9subject
Has Abstractpub_date
2019-06-25 00:00:00pages
9276issue
1issn
2045-2322pii
10.1038/s41598-019-45635-9journal_volume
9pub_type
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