Perrine Friedel

TL;DR: Recent advances in the understanding of the mechanisms regulating KCC2 activity are discussed, and of the role these mechanisms play in neuronal Cl− homeostasis and GABAergic neurotransmission are discussed.

TL;DR: The report of two non‐synonymous functional variants in human KCC2, R952H and R1049C, exhibiting clear statistical association with idiopathic generalized epilepsy (IGE) are described and suggest genetically encoded impairment of K CC2 functional regulation may be a risk factor for the development of human IGE.

TL;DR: Insight is provided into the mechanism regulating Cl− homeostasis in immature neurons, and it is suggested that WNK1-regulated changes in KCC2 phosphorylation contribute to the developmental excitatory-to-inhibitory GABA sequence.

TL;DR: Cryo-electron microscopy structures of the two neuronal cation-chloride cotransporters human NKCC1 and mouse KCC2 are presented, identifying their essential residues for ion transport and mechanisms by which phosphorylation regulates transport activity are proposed.

TL;DR: It is demonstrated that proBDNF impairs GABAergic transmission by the activation of two distinct pathways: a RhoA-Rock-PTEN pathway that decreases the phosphorylation levels of GABAAR, thus affecting receptor function and triggering endocytosis and degradation of internalized receptors, and a JAK-STAT-ICER pathway leading to the repression ofGAARs synthesis.