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Intracellular chloride accumulation: a possible mechanism for cognitive deficits in Down syndrome

A study involving a mouse model of Down syndrome and analysis of human postmortem brain samples indicates that hippocampal GABAA receptor signaling in Down syndrome may be excitatory. This advance promises new clinical applications in Down syndrome.

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Figure 1: Schematic model of GABAA receptor–mediated neurotransmission in a mouse model of DS.

Kim Caesar/Nature Publishing Group

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Correspondence to Alberto C Costa.

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Costa, A. Intracellular chloride accumulation: a possible mechanism for cognitive deficits in Down syndrome. Nat Med 21, 312–313 (2015). https://doi.org/10.1038/nm.3836

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