KCC2 downregulation after sciatic nerve injury enhances motor function recovery.

Injury to mature neurons induces downregulated KCC2 expression and activity, resulting in elevated intracellular [Cl] and depolarized GABAergic signaling. This phenotype mirrors immature neurons wherein GABA-evoked depolarizations facilitate neuronal circuit maturation. Thus, injury-induced KCC2 downregulation is broadly speculated to similarly facilitate neuronal circuit repair.

Overexpression of neuronal K-Cl co-transporter enhances dendritic spine plasticity and motor learning.

The neuronal K-Cl cotransporter KCC2 maintains a low intracellular Cl concentration and facilitates hyperpolarizing GABA receptor responses. KCC2 also plays a separate role in stabilizing and enhancing dendritic spines in the developing nervous system. Using a conditional transgenic mouse strategy, we examined whether overexpression of KCC2 enhances dendritic spines in the adult nervous system and characterized the effects on spine dynamics in the motor cortex in vivo during rotarod training.