期刊
CURRENT BIOLOGY
卷 27, 期 8, 页码 1111-1123出版社
CELL PRESS
DOI: 10.1016/j.cub.2017.02.065
关键词
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资金
- VIB
- NERF
- VIB International PhD Program
- ERC [335561]
- BELSPO WiBrain Interuniversity Attraction Pole [P7/20]
- FWO [G.0871.12N, G.0503.12]
- EMBO grant ALTF [1591-2014]
- European Commission [656824]
- Kavli Institute for Systems Neuroscience at NTNU
- Institut Hospitalier Universitaire (IHU)
- Institut du Cerveau et de la Moelle Epiniere (ICM)
- Paul G. Allen Frontiers Group
- Einstein Foundation
- FENS-Kavli Network of Excellence
- Marie Curie Actions (MSCA) [656824] Funding Source: Marie Curie Actions (MSCA)
Fragile X syndrome (FXS) patients present neuronal alterations that lead to severe intellectual disability, but the underlying neuronal circuit mechanisms are poorly understood. An emerging hypothesis postulates that reduced GABAergic inhibition of excitatory neurons is a key component in the pathophysiology of FXS. Here, we directly test this idea in a FXS Drosophila model. We show that FXS flies exhibit strongly impaired olfactory behaviors. In line with this, olfactory representations are less odor specific due to broader response tuning of excitatory projection neurons. We find that impaired inhibitory interactions underlie reduced specificity in olfactory computations. Finally, we show that defective lateral inhibition across projection neurons is caused by weaker inhibition from GABAergic interneurons. We provide direct evidence that deficient inhibition impairs sensory computations and behavior in an in vivo model of FXS. Together with evidence of impaired inhibition in autism and Rett syndrome, these findings suggest a potentially general mechanism for intellectual disability.
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