ArticleEpilepsia2026
Abnormal KCC2 expression and function in a mouse model of epilepsy and tuberous sclerosis complex.
Article in Epilepsia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveDrug-resistant epilepsy is a common, severe manifestation of the genetic disorder tuberous sclerosis complex (TSC). Although significant mechanistic and therapeutic advances have been made in TSC, treatments for seizures remain largely ineffective. Decreased expression of the potassium-chloride cotransporter KCC2 is associated with depolarizing γ-aminobutyric acid (GABA) signaling and increased neuronal excitability in the immature brain and in certain pathological states. In this study, we investigated abnormalities in KCC2 expression and function in a mouse model of TSC-related epilepsy.
methodsTsc1
resultsKCC2 expression was decreased in Tsc1 SIGNIFICANCE: Decreased KCC2 expression may lead to impaired GABAergic inhibition and increased neuronal excitability, contributing to epileptogenesis in TSC. Potentiation of KCC2 expression may represent a novel, effective therapeutic approach for epilepsy in TSC.
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