Sustained neuronal activity generated by glial plasticity

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Abstract

Astrocytes release gliotransmitters, notably glutamate, that can affect neuronal and synaptic activity. In particular, astrocytic glutamate release results in the generation of NMDA receptor (NMDA-R)-mediated slow inward currents (SICs) in neurons. However, factors underlying the emergence of SICs and their physiological roles are essentially unknown. Here we show that, in acute slices of rat somatosensory thalamus, stimulation of lemniscal or cortical afferents results in a sustained increase of SICs in thalamocortical (TC) neurons that outlasts the duration of the stimulus by 1 h. This long-term enhancement of astrocytic glutamate release is induced by group I metabotropic glutamate receptors and is dependent on astrocytic intracellular calcium. Neuronal SICs are mediated by extrasynaptic NR2B subunit-containing NMDA-Rs and are capable of eliciting bursts. These are distinct from T-type Ca2+ channel-dependent bursts of action potentials and are synchronized in neighboring TC neurons. These findings describe a previously unrecognized form of excitatory, nonsynaptic plasticity in the CNS that feeds forward to generate local neuronal firing long after stimulus termination.

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Original languageEnglish
Article number21613477
Pages (from-to)7637-7647
Number of pages10
JournalJournal of Neuroscience
Volume31
Issue number21
DOIs
Publication statusPublished - 25 May 2011

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Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported license

    Keywords

  • action potentials, afferent pathways, animals, male, neuroglia, neuronal plasticity, neurons, rats, Wistar rats, time factors

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