Corticothalamic feedback can force intact thalamic circuits into paroxysmal oscillations at 3 Hz.
Damien Debay, Alain Destexhe, Kirsty Grant and Thierry Bal

Society for Neuroscience Abstracts 25: 1167, 1999.

Many studies have stressed the importance of lateral inhibition between thalamic reticular cells in generating paroxysmal activity in thalamic circuits. By using in vitro electrophysiology in combination with computational models, we explored the possibility that corticothalamic feedback also has a determinant effect on thalamic oscillations, which may lead to paroxysmal discharges. Recordings were performed in ferret thalamic slices containing interconnected LGN and PGN layers. Corticothalamic feedback was mimicked by using the discharge of LGN cells to trigger stimulation of the optic radiation (OR). Antidromic activation of LGN cells was rarely observed. The effect of OR stimulation was highly dependent on intensity: single shocks entrained the network in a 10 Hz spindle rhythmicity, whereas stimuli consisting of 5-6 shocks at 100-200 Hz (Fig.) slowed the rhythm to about 3 Hz. Local application of CGP35348, a GABA-B blocker, reversed this forced 3 Hz rhythm back to spindle rhythmicity. The same protocol was simulated using computational models of thalamic circuits comprising Hodgkin-Huxley models of voltage-dependent currents (IT, Ih, INa, IK) and kinetic models of synaptic receptors (AMPA, GABA-A, GABA-B). Replication of the experimental results required two assumptions: (a) that GABA-B receptor-mediated responses are sensitive to the number of presynaptic spikes; (b) that corticothalamic EPSPs are more effective in causing the firing of PGN cells than LGN cells. In conclusion, these experiments and models show that intact thalamic circuits can be forced into 3 Hz paroxysmal oscillations by corticothalamic feedback. Supported by CNRS and Electricité Santé (France) and the MRC (Canada).