The role of thalamic IGABAB in generating spike-wave discharges during petit mal seizures.

Recent studies have suggested that 7-14 Hz spindle rhythms which appear during slow wave sleep and the 3 Hz spike-wave discharge accompanying petit mal seizures share common thalamocortical circuitry. A computational model was used to investigate the manner in which differential changes in the synaptic currents, IGABAA and IGABAB, observed in these cells can transform normal sleep spindles into the pathological oscillations recorded in primate exhibiting generalized petit mal epilepsy. The model suggests that inhibition by GABAergic interneurons and possibly nucleus reticularis thalami cells which reduce IGABA, increases the amplitude of the slower IGABAB. These events produce an extended inhibitory period in relay cells and also lead to the exaggerated post-inhibitory rebound Ca(2+)-dependent burst observed during seizures.