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- W2890591065 startingPage "126" @default.
- W2890591065 abstract "GABAergic synaptic inhibition, which is a critical regulator of neuronal excitability, is closely involved in epilepsy. Interestingly, fast GABAergic transmission mediated by Cl− permeable GABAA receptors can bi-directionally exert both seizure-suppressing and seizure-promoting actions. Accumulating evidence suggests that chloride plasticity, the driving force of GABAA receptor-mediated synaptic transmission, contributes to the double-edged role of GABAergic synapses in seizures. Large amounts of Cl− influx can overwhelm Cl− extrusion during seizures not only in healthy tissue in a short-term “activity-dependent” manner, but also in chronic epilepsy in a long-term, irreversible “pathology-dependent” manner related to the dysfunction of two chloride transporters: the chloride importer NKCC1 and the chloride exporter KCC2. In this review, we address the importance of chloride plasticity for the “activity-dependent” and “pathology-dependent” mechanisms underlying epileptic events and provide possible directions for further research, which may be clinically important for the design of GABAergic synapse-targeted precise therapeutic interventions for epilepsy." @default.
- W2890591065 created "2018-09-27" @default.
- W2890591065 creator A5018863416 @default.
- W2890591065 creator A5036865333 @default.
- W2890591065 creator A5074487340 @default.
- W2890591065 date "2018-12-01" @default.
- W2890591065 modified "2023-10-16" @default.
- W2890591065 title "Double-edged GABAergic synaptic transmission in seizures: The importance of chloride plasticity" @default.
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