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- W2031743812 endingPage "e1000492" @default.
- W2031743812 startingPage "e1000492" @default.
- W2031743812 abstract "Networks of specific inhibitory interneurons regulate principal cell firing in several forms of neocortical activity. Fast-spiking (FS) interneurons are potently self-inhibited by GABAergic autaptic transmission, allowing them to precisely control their own firing dynamics and timing. Here we show that in FS interneurons, high-frequency trains of action potentials can generate a delayed and prolonged GABAergic self-inhibition due to sustained asynchronous release at FS-cell autapses. Asynchronous release of GABA is simultaneously recorded in connected pyramidal (P) neurons. Asynchronous and synchronous autaptic release show differential presynaptic Ca2+ sensitivity, suggesting that they rely on different Ca2+ sensors and/or involve distinct pools of vesicles. In addition, asynchronous release is modulated by the endogenous Ca2+ buffer parvalbumin. Functionally, asynchronous release decreases FS-cell spike reliability and reduces the ability of P neurons to integrate incoming stimuli into precise firing. Since each FS cell contacts many P neurons, asynchronous release from a single interneuron may desynchronize a large portion of the local network and disrupt cortical information processing." @default.
- W2031743812 created "2016-06-24" @default.
- W2031743812 creator A5008789500 @default.
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- W2031743812 creator A5068886910 @default.
- W2031743812 creator A5082613410 @default.
- W2031743812 creator A5087948193 @default.
- W2031743812 date "2010-09-28" @default.
- W2031743812 modified "2023-10-18" @default.
- W2031743812 title "Desynchronization of Neocortical Networks by Asynchronous Release of GABA at Autaptic and Synaptic Contacts from Fast-Spiking Interneurons" @default.
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