Figure 4.

Extracellular recordings from PF neurons during HPDs. A₁, Microphotograph of a PF neuron labeled by juxtacellular injection of neurobiotin. The cell body (filled circle in the inset, schematic coronal plane drawing) was located in the central region of the lateral part of the PF nucleus. Anteriority from the interaural line was 1.62 mm. Fr, Fasciculus retroflexus; Po, posterior thalamic nucleus; VPM, ventral posteromedial thalamic nucleus. Scale bar, 100 μm. A₂–A₄, Single-spike activity of thalamic neurons (bottom traces) during paroxysmal activity in the ipsilateral hippocampus (top traces). A₂, Disruption of the spontaneous extracellular activity of the PF neuron shown in A₁ during the HPD (between the dashed vertical lines) and representative of the first subpopulation of PF cells. A₃, Extracellular activity of another PF neuron affected by the HPD occurrence and representative of the second subpopulation of PF cells. No change in their firing rate was observed. A₄, Simultaneous recording of two centrolateral thalamic nucleus (CL) neurons during HPD. Note that the activity of these two cells is not affected by the HPD. B₁–B₄, Mean cumulative histograms of binned action potential discharge of 19 PF neurons aligned to hippocampal epileptic events (5 s before and after the start of short clusters of isolated spikes (B₁, B₃) and HPDs (B₂, B₄). Note slight decrease of the activity of PF neurons after the beginning of hippocampal clusters of isolated spikes (B₁) or HPDs (B₃). Contrarily, the mean firing rate of PF neurons increased 500 ms before the end of cluster of isolated spikes (B₂) and HPDs (B₄) and lasted approximately 1.5 s after the end of hippocampal paroxysms.