Thalamocortical neuronal oscillations underlie various field potentials that are expressed in the neocortex, including sleep spindles and high voltage spike-and-wave patterns (HVSs). The mechanism of extracellular current generation in the neocortex was studied in the anesthetized and awake rat. Field potentials and unit activity were recorded simultaneously along trajectories perpendicular to the cortical layers at spatial intervals of 100 m by multiple-site recording silicon probes. Current source density (CSD) analysis revealed that the spatial positions of sinks in layers IV, V-VI, and II-III and of the accompanying sources were similar during sleep spindles, HVSs, and thalamic-evoked responses, although their relative strengths and timings differed. The magnitude and relative timing of the multiple pairs of sinks and sources determined the amplitude variability of HVSs and sleep spindles. The presence of temporally shifted dipoles was also supported by the time distribution of unit discharges in different layers. Putative interneurons discharged with repetitive bursts of 300-500 Hz. The spike component of HVSs was associated with fast field oscillations (400-600 Hz "ripples"). Discharges of pyramidal cells were phase-locked to the ripples. These findings indicate that the major extracellular currents underlying sleep spindles, HVSs, and evoked responses result from activation of intracortical circuitries. We hypothesize that the fast field ripples reflect summed IPSPs in pyramidal cells resulting from the high frequency barrage of interneurons.

The invasion of fast (Na+) spikes from the soma into dendrites was studied in single pyramidal cells of the sensorimotor cortex by simultaneous extracellular recordings of the somatic and dendritic action potentials in freely behaving rats. Field potentials and unit activity were monitored with multiple-site silicon probes along trajectories perpendicular to the cortical layers at spatial intervals of 100 micron. Dendritic action potentials of individual layer V pyramidal neurons could be recorded up to 400 micron from the cell body. Action potentials were initiated at the somatic recording site and traveled back to the apical dendrite at a velocity of 0.67 m/s. Current source density analysis of the action potential revealed time shifted dipoles, supporting the view of active spike propagation in dendrites. The presented method is suitable for exploring the conditions affecting the somadendritic propagation action of potentials in the behaving animal.

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Neocortical high-voltage spike-and-wave discharges (HVS) in the rat are an animal model of petit mal epilepsy. Genetic analysis of total duration of HVS (s/12 hr) in reciprocal F1 and F2 hybrids of F344 and BN rats indicated that the phenotypic variability of HVS cannot be explained by a simple, monogenic Mendelian model. Biometrical analysis suggested the presence of additive, dominance, and sex-linked-epistatic effects, buffering maternal influence, and heterosis. High correlation was observed between average duration (s/episode) and frequency of occurrence of spike-and-wave episodes (n/12 hr) in parental and segregating generations, indicating that common genes affect both duration and frequency of the spike-and-wave pattern. We propose that both genetic and developmental-environmental factors control an underlying quantitative variable, which, above a certain threshold level, precipitates HVS discharges. These findings, together with the recent availability of rat DNA markers for total genome mapping, pave the way to the identification of genes that control the susceptibility of the brain to spike-and-wave discharges.