Localization of the Origin of Self‐Sustained Afterdischarges (SSADs) in the Rat

Abstract

The genesis of the thalamocortical self-sustained afterdischarge (SSAD) composed of spike-and-wave (S + W) rhythm was studied in adult male albino rats. Under control conditions, rhythmic electrical stimulation of the specific somatosensory nucleus of the thalamus always elicited type S + W SSAD. An electrolytic lesion of the nonspecific thalamic nuclei did not prevent generation of type S + W SSAD, while stimulation of the ventrobasal complex evoked both type S + W SSAD and another type of SSAD composed of large waves with superimposed fast activity. Elimination of the cortex (by suction or spreading depression) ipsilateral to the stimulated thalamus completely suppressed any possibility of the formation of type S + W SSAD; elimination of the contralateral cortex did not affect it. Our results suggest that the cortex is the decisive factor in the genesis of S + W rhythm, while the thalamus markedly influences the conditions of its formation.

An Antagonist of GABA-B Receptors Potentiates Activity of Cortical Epileptic Foci

“…It is in agreement with our older finding that administration of an antagonist of GABA-B receptors CGP35348 results in marked prolongation of cortical afterdischarges in adult rats (Mareš et al 2007). Epileptic afterdischarges characterized by spike-and-wave rhythm in the EEG and clonic seizures are generated in the corticothalamic system (Pohl et al 1986). It is in agreement with mechanisms of generation of spike-and-wave rhythm generally (Avanzini et al 1992, Meeren et al 2002.…”

Anticonvulsant Action of GluN2A-Preferring Antagonist PEAQX in Developing Rats

“…The three seizure types used in our study are generated in different brain structures with different courses of maturation. PTZ-induced generalized tonic-clonic seizures are primarily generated in the brainstem [21,22] and spike-and-wave discharges characteristic for CxAD represent a corticothalamocortical phenomenon [23,36]. Minimal clonic seizures present after PTZ administration since the third postnatal week in rats (probably generated in basal forebrain [21,22]) were not markedly affected by PEAQX.…”