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
Abstract:
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.
return to
publication list
return to main page