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Bumetanide for autism: More eye contact, less amygdala activation

Journal article
Authors Nouchine Hadjikhani
Jakob Åsberg Johnels
A. Lassalle
N. R. Zürcher
L. Hippolyte
Christopher Gillberg
E. Lemonnier
Y. Ben-Ari
Published in Scientific Reports
Volume 8
Issue 1
ISSN 2045-2322
Publication year 2018
Published at Gillberg Neuropsychiatry Centre
Language en
Links doi.org/10.1038/s41598-018-21958-x
Subject categories Psychiatry, Neurosciences

Abstract

We recently showed that constraining eye contact leads to exaggerated increase of amygdala activation in autism. Here, in a proof of concept pilot study, we demonstrate that administration of bumetanide (a NKCC1 chloride importer antagonist that restores GABAergic inhibition) normalizes the level of amygdala activation during constrained eye contact with dynamic emotional face stimuli in autism. In addition, eye-tracking data reveal that bumetanide administration increases the time spent in spontaneous eye gaze during in a free-viewing mode of the same face stimuli. In keeping with clinical trials, our data support the Excitatory/Inhibitory dysfunction hypothesis in autism, and indicate that bumetanide may improve specific aspects of social processing in autism. Future double-blind placebo controlled studies with larger cohorts of participants will help clarify the mechanisms of bumetanide action in autism. © 2018 The Author(s).

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