RT Journal Article
SR Electronic
T1 Sustained Neuronal Activity Generated by Glial Plasticity
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 7637
OP 7647
DO 10.1523/JNEUROSCI.5783-10.2011
VO 31
IS 21
A1 Tiina M. Pirttimaki
A1 Stephen D. Hall
A1 H. Rheinallt Parri
YR 2011
UL http://www.jneurosci.org/content/31/21/7637.abstract
AB 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.