Fig. 4.

Synchronization of thalamic cells by the corticothalamic loop. A, Scheme showing the locations of the intracellular recordings that were done successively for the LGN cell and the PGN cell in the same slice, on an anteroposterior axis passing between the branches of the stimulating electrode (the likely orientation for the thalamocortical (TC)–PGN reciprocal connections). Multiunit recordings made at location indicated by thefilled circle. For both cells, stimulation parameters were kept identical (27 μA intensity; 4 shocks at 100 Hz).B, Simultaneous intracellular and multiunit (filled circle) recordings in the LGN during a spindle wave. C, Same recordings during a slow network activity resulting from cortical feedback stimulations (50 msec delay) triggered by the action potentials in the intracellular recording.D, Control multiunit recording in the PGN (spindle wave) and its transformation during cortical feedback stimulation (6 shocks at 100 Hz, 30 msec delay). An extracellular single-unit thalamocortical cell, recorded with another electrode, was the trigger of the feedback (data not shown). The integrated trace shows the amplification of the population bursts (arrows) compared to control (asterisk), indicative of an enhanced synchrony of the activity of PGN cells. E, Intracellular recording of a PGN cell during spontaneous spindle waves and OR stimulation imposed periodically, but this time without feedback (4 shocks at 100 Hz, 400 msec interstimulus interval). Arrows show the EPSPs originated from the rebound firing of thalamocortical cells in adjacent layers. F, Detail of these compound EPSPs and their averages (G) during spindle (top trace; n = 83; triggered on the first spike of the burst) and OR stimulations delivered at 500 msec intervals (bottom trace; n = 56; triggered on the first EPSP). For the average, only EPSPs not leading to the generation of low-threshold calcium spike and bursting were selected.