Fig. 8.

Thalamocortical relationships in rat H16.A, Distribution of the overall thalamocortical time delays (= time delay when whole seizure is analyzed as one epoch) for individual seizures (n = 10) for the combinations of cortical and thalamic sites, which were shown to be interconnected as indicated by the black and grayarrows in the schematic drawing on theright. The time delays τ (in milliseconds) are bimodally distributed with both positive and negative delays, corresponding to either thalamus “leading” orcortex “leading.”B, Thalamocortical association strengths and time delays for the 500 msec epochs during the transition to a seizure for the electrode pair with a cortical focus (Th-B4 and Cx-f), indicated by the black arrow in the schematic drawing underA. The left panel shows theh²(τ) plots (association as a function of time delay) for three successive 50% overlapping epochs during a single seizure. Time point 0 indicates the onset of the seizure (appearance of the first generalized spike). During the first 500 msec of the seizure, the h²(τ) plot is characterized by a clear maximum at a negative time delay, indicating that the cortex is leading. In the successive epochs, a maximum at a positive time delay, corresponding to thalamus leading, appears. During the second 500 msec of the seizure the latter maximum has become larger than the former maximum. The right panel shows the time evolution of the average association parameters over seizures (mean ± SEM; n = 10 seizures) during the transition phase. Values belonging to a given epoch are plotted at the mid time point of the corresponding epoch (for example, values plotted at t = 0.5 are derived from the 250–750 msec epoch). A steady rise in the strength of association can be noticed at the top. At thebottom, before onset of the seizure there is a large variation in time delay. During the first 500 msec of the seizure, however (time point 0.25 sec; epoch 0–500 msec), this variation decreases to almost zero, resulting in a significant negative time delay, which signifies that the cortex consistently leads the thalamus. After this first seizure epoch the variation in time delay increases again, resulting in values that do not differ significantly from zero.