Preoptic area controls sleep-related seizure onset in a genetic epilepsy mouse model.

In genetic and refractory epileptic patients, seizure activity exhibits sleep-related modulation/regulation and sleep and seizure are intermingled. In this study, by using one het KI mice as a genetic epilepsy model and optogenetic method , we found that subcortical POA neurons were active within epileptic network from the het KI mice and the POA activity preceded epileptic (poly)spike-wave discharges(SWD/PSDs) in the het KI mice. Meanwhile, as expected, the manipulating of the POA activity relatively altered NREM sleep and wake periods in both wt and the het KI mice.

Sleep slow-wave oscillations trigger seizures in a genetic epilepsy model of Dravet syndrome.

Sleep is the preferential period when epileptic spike-wave discharges appear in human epileptic patients, including genetic epileptic seizures such as Dravet syndrome with multiple mutations including SCN1A mutation and GABA receptor γ2 subunit Gabrg2 mutation in patients, which presents more severe epileptic symptoms in female patients than male patients. However, the seizure onset mechanism during sleep still remains unknown. Our previous work has shown that the sleep-like state-dependent homeostatic synaptic potentiation can trigger epileptic spike-wave discharges in one transgenic heterozygous knock-in mouse model.

Artificial sleep-like up/down-states induce synaptic plasticity in cortical neurons from mouse brain slices.

During non-rapid eye movement (NREM) sleep, cortical neuron activity alternates between a depolarized (firing, up-state) and a hyperpolarized state (down-state) coinciding with delta electroencephalogram (EEG) slow-wave oscillation (SWO, 0. 5-4 Hz) . Recently, we have found that artificial sleep-like up/down-states can potentiate synaptic strength in layer V cortical neurons .