KCC2 drives chloride microdomain formation in dendritic blebbing

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/36288701

Research summary

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.

Key outcome of the study

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.

Mouse model

KCC2 Knockin point mutation mouse model, engineered to assess the functional effects of a specific amino acid substitution in the KCC2 transporter.

TARGET:
SLC12A5
KCC2

Keywords

Neurodegeneration, Excitotoxicity, Chloride homeostasis, Dendritic injury, Ion transport

Technical specifications

Knockin model, Point mutation, KCC2 functional alteration, Electrophysiology, Fluorescent chloride imaging

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Point mutation KI mouse

Use a point mutation mouse Knockin to circumvent complex phenotypes arising from complete Knockouts (e.g., signaling pathway problems, cross-reactivity).