Spike-Wave Complexes and Fast Components of Cortically Generated Seizures. II. Extra- and Intracellular Patterns

Abstract

In the previous paper we have demonstrated, by means of field potential and extracellular unit recordings, that bicuculline-induced seizures, which include spike-wave (SW) or polyspike-wave (PSW) complexes, are initiated intracortically and survive ipsilateral thalamectomy. Here, we used multisite field potential and extracellular recordings to validate the patterns of cortical SW/PSW seizures in chronically implanted, behaving cats. To investigate the cellular patterns and excitability during spontaneously occurring and electrically elicited cortical seizures, we used single and dual intracellular recordings from regular-spiking (RS) and fast-rhythmic-bursting (FRB) cortical neurons, in conjunction with field potential recordings from neocortex and related thalamic nuclei, in cats maintained under ketamine-xylazine anesthesia. 1) Invariably, the spontaneous or electrically induced seizures were initiated within the cortex of both behaving and anesthetized animals. Spontaneously occurring, compound seizures consisting of SW/PSW complexes at 2-4 Hz and fast runs at 10-15 Hz, developed without discontinuity from the slow (mainly 0.5-0.9 Hz), sleeplike, cortically generated oscillation. 2) During SW/PSW complexes, RS neurons discharged spike trains during the depth-negative component of the cortical "spike" component of field potentials and were hyperpolarized during the depth-positive field wave. The FRB neurons fired many more action potentials than RS cells during SW/PSW complexes. Averaged activities triggered by the spiky field potentials or by the steepest slope of depolarization in cortical neurons demonstrated similar relations between intracellular activities and field potentials during sleep and seizure epochs, the latter-being an exaggeration of the depolarizing and hyperpolarizing components of the slow sleep oscillation. 3) During the fast runs, RS cells were tonically depolarized and discharged single action potentials or spike doublets (usually with pronounced spike inactivation), whereas FRB cells discharged rhythmic spike bursts, time locked with the depth-negative field potentials. 4) Neuronal excitability, tested by depolarizing current pulses applied throughout the seizures and compared with pre- and postseizure epochs, showed a decreased number of evoked action potentials during both seizure components (SW/PSW complexes and fast runs), eventually leading to null responses during the postictal depression. 5) Data suggest that interconnected FRB neurons may play an important role in the initiation of cortical seizures. We discuss the similarities between the electrographic patterns described in this study and those found in different forms of clinical seizures.

Sensorimotor cortical influences on cuneate nucleus rhythmic activity in the anesthetized cat

“…2A), and thus the rapid monosynaptic excitation of CLs, together with post-inhibitory rebound potentials, probably induced through interneurons, explain the synchronization observed between the "spike" of the ECoG and the gross lemniscal activity ( Figs 7B, 8C, left panel). It has been demonstrated that the fast-rhythmic bursting cortical neurons contribute to the initiation of spontaneous and electrically elicited spike-and-wave cortical paroxysms, 44 and since the axons of these cells reach the cuneate (Fig. 2B), they might be responsible for the initial powerful excitatory effects exerted by the cerebral cortex on CLs, as reported previously.…”

Inactivation of Calcium-Binding Protein Genes Induces 160 Hz Oscillations in the Cerebellar Cortex of Alert Mice

“…LFPs were analyzed by the wave-triggered average (WTA) technique (Steriade et al, 1998) and the fast Fourier transform algorithm. An oscillation index was computed as peak amplitude divided by total power.…”

Conditional Bursting Enhances Resonant Firing in Neocortical Layer 2–3 Pyramidal Neurons

“…Neocortical oscillations at ϳ10 Hz are observed in vivo and in brain slices under conditions of enhanced excitability (Silva et al, 1991;Flint and Connors, 1996;Lukatch and MacIver, 1997;Steriade et al, 1998b;Castro-Alamancos, 2000, 2006Castro-Alamancos and Rigas, 2002;Castro-Alamancos et al, 2007). Oscillations at 10 Hz occur while GABA receptors are blocked (Flint and Connors, 1996), suggesting that they are generated by the excitatory network.…”