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Science. 2014 Oct 10;346(6206):176. doi: 10.1126/science.1256009.

Response to Comment on "Oxytocin-mediated GABA inhibition during delivery attenuates autism pathogenesis in rodent offspring".

Author information

1
Mediterranean Institute of Neurobiology (INMED), U901, INSERM, Marseille, France. UMR 901, Aix-Marseille University, Marseille, France. Neurochlore, Campus Scientifique de Luminy, 163 Route de Luminy, Marseille, France. On leave from Iran University of Medical Sciences, Tehran, Iran.
2
Mediterranean Institute of Neurobiology (INMED), U901, INSERM, Marseille, France. UMR 901, Aix-Marseille University, Marseille, France. Neurochlore, Campus Scientifique de Luminy, 163 Route de Luminy, Marseille, France. On leave from Tehran University of Medical Sciences, Tehran, Iran.
3
Mediterranean Institute of Neurobiology (INMED), U901, INSERM, Marseille, France. UMR 901, Aix-Marseille University, Marseille, France.
4
Neurochlore, Campus Scientifique de Luminy, 163 Route de Luminy, Marseille, France.
5
Mediterranean Institute of Neurobiology (INMED), U901, INSERM, Marseille, France. UMR 901, Aix-Marseille University, Marseille, France. Neurochlore, Campus Scientifique de Luminy, 163 Route de Luminy, Marseille, France. yehezkel.ben-ari@inserm.fr.

Abstract

Bambini-Junior et al. questioned whether our treatment in two rodent models of autism has a long-lasting effect into adulthood. In response, we show that bumetanide treatment around delivery attenuates autistic behavioral features in adult offspring. Therefore, the polarity of γ-aminobutyric acid (GABA) actions during delivery exerts long-lasting priming actions after birth.

PMID:
25301611
DOI:
10.1126/science.1256009
[Indexed for MEDLINE]
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