Early alterations in a mouse model of Rett syndrome: the GABA developmental shift is abolished at birth.

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 Rep

journal_title

Scientific reports

authors

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 Y

doi

10.1038/s41598-019-45635-9

subject

Has Abstract

pub_date

2019-06-25 00:00:00

pages

9276

issue

1

issn

2045-2322

pii

10.1038/s41598-019-45635-9

journal_volume

9

pub_type

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