Cortical drive and thalamic feed-forward inhibition control thalamic output synchrony during absence seizures
Résumé
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 Ca 2+ channels (T-channels)-dependent burst firing in thalamocortical (TC) neurons, and by temporally framing thalamic output via feed-forward reticular thalamic (NRT)-to-TC neuron inhibition. In TC neurons, overall ictal firing is markedly reduced and bursts rarely occur. Moreover, block of T-channels in cortical and NRT neurons suppresses ASs, but in TC neurons has no effect on seizures or on ictal thalamic output synchrony. These results demonstrate ictal bidirectional cortico-thalamic communications and provide the
Domaines
Neurobiologie
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