Identifying the neurons initiating absence seizure

In this article, we investigated the mechanisms of initiation and propagation of absence seizures in the GAERS, a rat genetic model of absence epilepsy. We showed that absence seizures are initiated in the deep layers (layers 5 and 6) of the somatosensory cortex before propagating to the entire cortico-thalamic loop. The ictogenic neurons (neurons initiating the seizures) were characterized by an hyperactivity in between seizures (intecictal periods) due to a more depolarized membrane potential. During seizures the ictogenic neurons were systematically leading the epileptic activities. Altogether, this article confirmed and extended the “focal hypothesis” of absence epilepsy and provided a cellular scenario for the initiation and generalization of absence seizures.

Specificity of the hyperactivity of focus deep layer neurons. A , Interictal and ictal intracellular activities recorded from layer 5 neurons from focus (top) and motor cortex (MoCx; bottom) in the same GAERS, simultaneously with the corresponding ECoGs (top trace). Note the dramatic lowering in the interictal and ictal firing rate in the motor neuron. B , Spontaneous intracellular activity of a somatosensory cortical neuron (SoCx; bottom) from a normal Wistar rat, simultaneously recorded with the local ECoG (top). The mean values of interictal membrane potential are −58, −64, and −62 mV in neurons from cortical focus, MoCx ( A ), and SoCx ( B ), respectively.