期刊
NATURE NEUROSCIENCE
卷 21, 期 5, 页码 744-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41593-018-0130-4
关键词
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资金
- MRC [G0900671]
- Wellcome Trust [91882, 93763, 204014]
- Hungarian Scientific Research Fund [NN125601]
- Hungarian Brain Research Program [KTIA_NAP_13-2-2014-0014]
- CNRS [LIA 528]
- European Union [COST Action CM1103]
- Malta Council of Science and Technology (MCST) [RI-2013-14]
- Marie Curie ITN PhD studentship [H2020-MSCA-ITN-2016-722053]
- MRC [G0900671] Funding Source: UKRI
Behaviorally and pathologically relevant cortico-thalamo-cortical oscillations are driven by diverse interacting cell-intrinsic and synaptic processes. However, the mechanism that gives rise to the paroxysmal oscillations of absence seizures (ASs) remains unknown. Here we report that, during ASs in behaving animals, cortico-thalamic excitation drives thalamic firing by preferentially eliciting tonic rather than T-type Ca2+ channel (T-channel)-dependent burst firing in thalamocortical (TC) neurons and by temporally framing thalamic output via feedforward reticular thalamic (NRT)-to-TC neuron inhibition. In TC neurons, overall ictal firing was markedly reduced and bursts rarely occurred. Moreover, blockade of T-channels in cortical and NRT neurons suppressed ASs, but such blockade in TC neurons had no effect on seizures or on ictal thalamic output synchrony. These results demonstrate ictal bidirectional cortico-thalamic communications and provide the first mechanistic understanding of cortico-thalamo-cortical network firing dynamics during ASs in behaving animals.
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