摘要：SummaryAbsence seizures, manifested by spike-wave discharges (SWD) in the electroencephalogram, display synchronous reciprocal excitation between the neocortex and thalamus. Recent studies have revealed that inhibitory neurons in the reticular thalamic (RT) nucleus and excitatory thalamocortical (TC) neurons are two subcortical players in generating SWD. However, the signals that drive SWD-related activity remain elusive. Here, we show that SWD predominately occurs during wakefulness in several mouse models of absence epilepsy. In more focused studies ofGnb1mutant mice, we found that sensory input regulates SWD. Usingin vivorecording, we demonstrate that TC cells are activated prior to the onset of SWD and then inhibited during SWD. On the contrary, RT cells are slightly inhibited prior to SWD, but are strongly activated during SWD. Furthermore, chemogenetic activation of TC cells leads to the enhancement of SWD. Together, our results indicate that sensory input can regulate SWD by activating the thalamocortical pathway.Graphical abstractDisplay OmittedHighlights•Brain states strongly regulate the occurrence of SWD•Sensory input during wakefulness increases SWD in Gnb1 mice•RT cells are activated, and TC cells are inhibited during SWD in Gnb1 mice•Chemogenetic activation of TC cells enhances SWD in Gnb1 miceBiological sciences; Neuroscience; Molecular neuroscience; Sensory neuroscience.
