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The Journal of Neurophysiology Vol. 79 No. 5 May 1998,
pp. 2730-2748
Copyright ©1998 The American Physiological Society
1 Howard Hughes Medical Institute, The Salk Institute, Computational Neurobiology Laboratory, La Jolla, California 92037; 2 Laboratory of Neurophysiology, School of Medicine, Laval University, Quebec G1K 7P4, Canada; and 3 Department of Biology, University of California San Diego, La Jolla, California 92093
Bazhenov, Maxim, Igor Timofeev, Mircea Steriade, and Terrence J. Sejnowski. Cellular and network models for intrathalamic augmenting responses during 10-Hz stimulation. J. Neurophysiol. 79: 2730-2748, 1998. Repetitive stimulation of the thalamus at7-14 Hz evokes responses of increasing amplitude in the thalamus and the areas of the neocortex to which the stimulated foci project. Possible mechanisms underlying the thalamic augmenting responses during repetitive stimulation were investigated with computer models of interacting thalamocortical (TC) and thalamic reticular (RE) cells. The ionic currents in these cells were modeled with Hodgkin-Huxley type of kinetics, and the results of the model were compared with in vivo thalamic recordings from decorticated cats. The simplest network model demonstrating an augmenting response was a single pair of coupled RE and TC cells, in which RE-induced inhibitory postsynaptic potentials (IPSPs) in the TC cell led to progressive deinactivation of a low-threshold Ca2+ current. The augmenting responses in two reciprocally interacting chains of RE and TC cells depended also on
-aminobutyric acid-B (GABAB) IPSPs. Lateral GABAA inhibition between identical RE cells, which weakened bursts in these cells, diminished GABAB IPSPs and delayed the augmenting response in TC cells. The results of these simulations show that the interplay between existing mechanisms in the thalamus explains the basic properties of the intrathalamic augmenting responses.
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