Figure 3. Intracellular activity of PF thalamic neurons is disrupted by hippocampal seizures in vivo. A, Electrophysiological properties of recorded PF thalamic neurons. A1, Voltage responses (top traces) of a PF thalamic neuron to hyperpolarizing (average potential from 10 successive trials) and depolarizing (single-response) current pulses (bottom traces). Note the tonic firing induced by the positive current and the postinhibitory excitatory rebound evidenced by the averaging of action potentials (arrow). A2, In these two other PF cells, the current-induced hyperpolarization was clearly followed by a robust postanodal excitation, reminiscent of a low-threshold calcium potential, crowned by a burst of sodium spikes. A sag potential, likely caused by the hyperpolarization-activated inward cationic current, could also detected in some cells (bottom, arrow). B, C, Disruption of the spontaneous intracellular activity of PF neurons (bottom trace) during paroxysmal activity in the ipsilateral hippocampal (Hipp.) LFP (top trace). B, The thalamic cell was slightly hyperpolarized during the epileptic episode, and its firing was transiently interrupted. A prolonged train of action potentials promptly followed the HPD. C, In this other neuron, the firing rate was decreased during the HPD and then dramatically augmented at the termination of hippocampal paroxysms (dashed boxes). D, The excitatory postictal rebound in PF neurons resulted from summed dPSPs. At the end of the HPD (top), the thalamic neuron, which was hyperpolarized by DC current injection (−1.0 nA; middle trace), displayed a sustained membrane depolarization. As shown by the expansion of the record segment (bottom) indicated by the asterisk, the excitatory rebound resulted from the temporal summation of individual dPSPs (oblique lines). Arrowheads indicate the mean interictal membrane potential.