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• W2023195612 abstract "KV2.1 is the prominent somatodendritic sustained or delayed rectifier voltage-gated potassium (Kv) channel in mammalian central neurons, and is a target for activity-dependent modulation via calcineurin-dependent dephosphorylation. Using hanatoxin-mediated block of KV2.1 we show that, in cultured rat hippocampal neurons, glutamate stimulation leads to significant hyperpolarizing shifts in the voltage-dependent activation and inactivation gating properties of the KV2.1-component of delayed rectifier K+ (IK) currents. In computer models of hippocampal neurons, these glutamate-stimulated shifts in the gating of the KV2.1-component of IK lead to a dramatic suppression of action potential firing frequency. Current-clamp experiments in cultured rat hippocampal neurons showed glutamate-stimulation induced a similar suppression of neuronal firing frequency. Membrane depolarization also resulted in similar hyperpolarizing shifts in the voltage-dependent gating properties of neuronal IK currents, and suppression of neuronal firing. The glutamate-induced effects on neuronal firing were eliminated by hanatoxin, but not by dendrotoxin-K, a blocker of KV1.1-containing channels. These studies together demonstrate a specific contribution of modulation of KV2.1 channels in the activity-dependent regulation of intrinsic neuronal excitability." @default.
• W2023195612 created "2016-06-24" @default.
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• W2023195612 date "2009-01-01" @default.
• W2023195612 modified "2023-10-06" @default.
• W2023195612 title "Regulation of intrinsic excitability in hippocampal neurons by activity-dependent modulation of the K_V2.1 potassium channel" @default.
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• W2023195612 doi "https://doi.org/10.4161/chan.3.1.7655" @default.
• W2023195612 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2743964" @default.
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