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• W2113971423 abstract "The efficacy of GABAergic synaptic inhibition is a principal factor in controlling neuronal activity. We demonstrate here that brain-derived neurotrophic factor modulates the activity of GABA A receptors, the main sites of fast synaptic inhibition in the brain, within minutes of application. Temporally, this comprised an early enhancement in the miniature IPSC amplitude, followed by a prolonged depression. This modulation was concurrent with enhanced PKC-mediated phosphorylation, followed by protein phosphatase 2A (PP2A)-mediated dephosphorylation of the GABA A receptor. Mechanistically, these events were facilitated by differential recruitment of PKC, receptor for activated C-kinase, and PP2A to GABA A receptors, depending on the phosphorylation state of the receptor β 3 -subunit. Thus, transient formation of GABA A receptor signaling complexes has the potential to provide a basis for acute changes in receptor function underlying GABAergic synaptic plasticity." @default.
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• W2113971423 date "2004-01-14" @default.
• W2113971423 modified "2023-10-16" @default.
• W2113971423 title "Brain-Derived Neurotrophic Factor Modulates Fast Synaptic Inhibition by Regulating GABA_AReceptor Phosphorylation, Activity, and Cell-Surface Stability" @default.
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• W2113971423 doi "https://doi.org/10.1523/jneurosci.3606-03.2004" @default.
• W2113971423 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6729993" @default.
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