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Furosemide prevents membrane KCC2 downregulation during convulsant stimulation in the hippocampus by Lulan Chen; Jiangning Yu; Li Wan; Zheng Wu; Guoxiang Wang; Zihan Hu; Liang Ren; Jing Zhou; Binbin Qian; Xuan Zhao; Jinwei Zhang; Xu Liu; Yun Wang is a Neuroscience article available to read on EtoBox.

What is Furosemide prevents membrane KCC2 downregulation during convulsant stimulation in the hippocampus about?

In adults, γ-aminobutyric acid (GABA) type A receptor (GABA~A~R)-mediated inhibition depends on the maintenance of low intracellular chloride anion concentration through neuron-specific potassium-chloride cotransporter-2 (KCC2). KCC2 has been widely reported to have a plasticity change during the course of epilepsy development, with an early downregulation and late recovery in neuronal cell membranes after epileptic stimulation, which facilitates epileptiform burst activity. Furosemide is a clinical loop diuretic that inhibits KCC2. Here, we first confirmed that furosemide pretreatment could effectively prevented convulsant stimulation-induced neuronal membrane KCC2 downregulation in the hippocampus in both in vivo and in vitro cyclothiazide-induced seizure model. Second, we verified that furosemide pretreatment rescued KCC2 function deficits, as indicated by __E__~GABA~ depolarizing shift and GABA~A~R inhibitory function impairment induced via cyclothiazide treatment. Further, we demonstrated that furosemide also suppressed cyclothiazide-induced epileptiform burst activity in cultured hippocampal neurons and lowered the mortality rate during acute seizure induction. Overall, furos

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Author

Lulan Chen; Jiangning Yu; Li Wan; Zheng Wu; Guoxiang Wang; Zihan Hu; Liang Ren; Jing Zhou; Binbin Qian; Xuan Zhao; Jinwei Zhang; Xu Liu; Yun Wang

Publisher

Elsevier BV

Published

2022

Language

EN

Field

Neuroscience (Life Sciences)