Year: 2018
Type: article
Abstract: extrusion, without altering total or plasma membrane accumulation of KCC2. Critically, activity-induced deficits in synaptic inhibition were reduced in the mutant mice. Consistent with this, enhanced KCC2 was sufficient to limit chemoconvulsant-induced epileptiform activity. Furthermore, this increase in KCC2 function mitigated induction of aberrant high-frequency activity during seizures, highlighting depolarizing GABA as a key contributor to the pathological neuronal synchronization seen in epilepsy. Thus, our results demonstrate that potentiating KCC2 represents a therapeutic strategy to alleviate seizures.
Language: English
Subfield: Psychiatry and Mental health
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
Awards: G1074715819, G1984206704, G3141692634, Deficits in KCC2 activity and the pathophysiology of Autism spectrum disorders, G3959604937, G4111421279, Dissecting Mechanisms of GABAB-GIRK Plasticity with Psychostimulants, G7037907492, G707860662, G7248041895, G734143236, G7411678401, G7709784172, G890191660, G9000160295, G9000334094
OpenAlex ID: W2890803446
