While several studies in rats showed no activity changes in visual cortex 8, or in somatosensory and motor cortex 9, functional magnetic resonance imaging (fMRI) studies in humans have demonstrated increased ictal blood oxygen level-dependent (BOLD) activity in the occipital cortex 10, or biphasic activation and deactivation of large scale networks, including visual cortex 11, 12. However, prior work in humans and animal models of absence epilepsy reveal inconsistent evidence of where and how cortical activity is modulated during seizures. This loss of inhibition, particularly feedforward inhibition, is implicated in the pathophysiology of most monogenic models of absence epilepsy 1, 7. Loss of the transmembrane AMPA receptor regulatory protein (TARP) subunit Cacng2 in stargazer mice leads to mistrafficking of dendritic AMPA receptors in fast-spiking interneurons in the neocortex 3 and thalamus 4, 5 and to remodeling of firing properties in thalamocortical circuitry that favor abnormal oscillations 6. The stargazer model, one of over 20 monogenic mouse mutants with this phenotype 1, displays frequent, recurrent spike-wave seizures with behavioral arrest that are sensitive to blockade by ethosuximide 2. The events provide unique functional insight into the coupling of human perception and volition, and the cellular basis of this seizure type is steadily emerging from the study of genetic mouse models. Each seizure begins without warning, replacing planned motor movements with speech arrest and a vacant stare lasting only a few seconds, followed by sudden and complete recovery of awareness and intentional behavior. Our results demonstrate asynchronous suppression of visual cortex during absence seizures, with potential implications for understanding cortical network function during EEG states of reduced awareness.Ībsence epilepsy interrupts normal cortical processing, producing reversible episodes of altered consciousness. Pairwise correlation analysis of calcium activity reveals a surprising lack of synchrony among neurons and neuropil patches in all layers during seizures. Unexpectedly, ictal participation of identified single-unit activity is not fixed, but fluctuates on a flexible time scale from seizure to seizure.

We show that most (~80%) neurons in all cortical layers reduce their activity during seizures, whereas a smaller pool activates or remains neutral.

Using the calcium indicator GCaMP6 with in vivo 2-photon cellular microscopy and simultaneous electrocorticography, we examined the collective activity profiles of individual neurons and surrounding neuropil across all layers in V1 during spike-wave seizure activity over prolonged periods in stargazer mice. Absence epilepsy is a common childhood disorder featuring frequent cortical spike-wave seizures with a loss of awareness and behavior.

Absence seizure eeg temporal