Nucleus reticularis thalami controls the quiescence of thalamocortical neurons during seizures in a computer network model.
William W. Lytton, Diego Contreras, Alain Destexhe and Mircea Steriade

Society for Neuroscience Abstracts 22: 2030, 1996.

Intracellular recordings from thalamocortical (TC) neurons during spontaneous seizures in a cat model of spike-wave epilepsy indicate a surprising preponderence (60%) of quiescent cells (Steriade and Contreras, J. Neurosci. 1995, 15:623-642). During these seizures, thalamic reticular (RE) cells produced long (150-300 ms) spike-bursts simultaneous to the paroxysmal “spikes” in cortical EEG, whereas TC neurons either exhibited quiescence with continuous synaptic bombardment or occasionally displayed low-threshold spikes in synchrony. Several computer models of simple 2-neuron (RE-TC) models were assessed to explore factors contributing to the maintenance of quiescence and to the transition between quiescence and bursting in TC cells. Generally, small increases in GABA_B strength tended to produce TC quiescence. We also demonstrate that such changes could result from cooperative kinetics of GABA_B activation via second messengers. Switching between quiescence and oscillatory mode in these models was shown to be related to the strength and to the precise timing of simulated cortical stimulation. In many cases, complex dynamics in the 2-neuron network gave extreme sensitivity to the precise phase of effective cortical inputs. The dynamics also permitted spontaneous switching between states. This study suggests that quiescent patterns of TC cells during spike-wave seizures can result from known intrinsic properties and synaptic interactions in the thalamic circuitry and emphasizes the important role of GABA_B receptors. Supported by NSF, MRC of Canada and Savoy Foundation.