Altered Cl⁻ homeostasis hinders forebrain GABAergic interneuron migration in a mouse model of intellectual disability

Impairments of inhibitory circuits are at the basis of most, if not all, cognitive deficits. The impact of OPHN1, a gene associate with intellectual disability (ID), on inhibitory neurons remains elusive. We addressed this issue by analyzing the postnatal migration of inhibitory interneurons derived...

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Veröffentlicht in:	Proceedings of the National Academy of Sciences - PNAS 2021-01, Vol.118 (2), p.1-12
Hauptverfasser:	Maset, Andrea, Galla, Luisa, Francia, Simona, Cozzolino, Olga, Capasso, Paola, Goisis, Rosa Chiara, Losi, Gabriele, Lombardo, Angelo, Ratto, Gian Michele, Lodovichi, Claudia
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Biological Sciences Brain Cell Movement - physiology Chlorides - metabolism Chlorides - physiology Cognitive ability Cytoskeletal Proteins - genetics Cytoskeletal Proteins - metabolism Forebrain GABAergic Neurons - metabolism GABAergic Neurons - physiology GTPase-Activating Proteins - genetics GTPase-Activating Proteins - metabolism Hippocampus Homeostasis Intellectual disabilities Intellectual Disability - metabolism Intellectual Disability - physiopathology Interneurons - metabolism Interneurons - physiology Male Mice Models, Animal Neural coding Neural networks Neural Stem Cells - metabolism Neurogenesis Nuclear Proteins - metabolism Prosencephalon - metabolism Retina rhoA GTP-Binding Protein - metabolism Signal Transduction Somatosensory cortex Spatial discrimination Visual cortex Visual field Visual fields Visual stimuli Visual system γ-Aminobutyric acid
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