We investigated in anesthetized cats the progressive development from EEG-synchronized sleep patterns to low-frequency (< 15 Hz) paroxysmal activities, most of them consisting of epileptic-like seizures with spike-wave (SW) complexes at 2–4 Hz. We used multisite extra- and intracellular recordings of neocortical, reticular thalamic (RE), and thalamocortical (TC) neurons, including dual impalements of cortical and TC cells. A subsample (40%) of TC cells discharged spike bursts at 2–4 Hz, in close time relation with the spiky, depth-negative field components of SW seizures in related neocortical areas. Full synchronization among TC cells that were resonant with the cortical seizure activity was progressively reached toward the end of the SW paroxysm. The remaining TC cells (60%) were inhibited during the cortical SW seizures. We show that the duration and amplitude of hyperpolarization in TC cells paralleled the extent of cortical EEG paroxysm. Dual intracellular recordings of cortical and TC neurons demonstrate that during the cortical SW seizure, consisting of a tonic depolarization with superimposed paroxysmal spike bursts, the simultaneously recorded TC neurons displayed a tonic hyperpolarization associated with repetitive IPSPs, closely time related with cortical cell bursts. The inhibition of TC cells was presumably mediated by GABAergic RE thalamic neurons. Indeed, simultaneously recorded RE and TC neurons during the cortical SW paroxysm showed that cortical and RE cell excitation was accompanied by corresponding IPSPs in TC cells. We emphasize the progressive development from sleep patterns to some forms of epileptic-like activities. We propose that the inhibitory processes found in a significant number of TC cells during cortical SW seizures may contribute to the loss of consciousness, due to obliteration of synaptic transmission through the thalamus.