This study investigates how the potassium-chloride cotransporter KCC2 contributes to the formation of chloride microdomains during dendritic blebbing, a process associated with neuronal injury. Researchers used a KCC2 Knockin mouse model bearing a point mutation that modifies transporter function. NMDA receptor activation was shown to cause localized chloride accumulation at dendritic blebs through reversed KCC2 transport, contributing to dendritic swelling.
NMDA receptor activation leads to localized chloride accumulation in dendritic blebs via SK channel activation and reversed KCC2 transport. The findings highlight a critical role for KCC2 in excitotoxic dendritic pathology.
KCC2 Knockin point mutation mouse model, engineered to assess the functional effects of a specific amino acid substitution in the KCC2 transporter.
Neurodegeneration, Excitotoxicity, Chloride homeostasis, Dendritic injury, Ion transport
Knockin model, Point mutation, KCC2 functional alteration, Electrophysiology, Fluorescent chloride imaging
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