CONTROL OF SLOW OSCILLATIONS IN THE THALAMOCORTICAL NEURON - A COMPUTER-MODEL

Citation
Ww. Lytton et al., CONTROL OF SLOW OSCILLATIONS IN THE THALAMOCORTICAL NEURON - A COMPUTER-MODEL, Neuroscience, 70(3), 1996, pp. 673-684
Citations number
51
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
03064522
Volume
70
Issue
3
Year of publication
1996
Pages
673 - 684
Database
ISI
SICI code
0306-4522(1996)70:3<673:COSOIT>2.0.ZU;2-M
Abstract
We investigated computer models of a single thalamocortical neuron to assess the interaction of intrinsic voltage-sensitive channels and cor tical synaptic input in producing the range of oscillation frequencies observed in these cells in vivo. A morphologically detailed model wit h Hodgkin-Huxley-like ion channels demonstrated that intrinsic propert ies would be sufficient to readily produce 3 to 6 Hz oscillations. Hyp erpolarization of the model cell reduced its oscillation frequency mon otonically whether through current injection or modulation of a potass ium conductance, simulating the response to a neuromodulatory input. W e performed detailed analysis of highly reduced models to determine th e mechanism of this frequency control. The interburst interval was con trolled by two different mechanisms depending on whether or not the pa cemaker current, I-H, was present. In the absence of I-H, depolarizati on during the interburst interval occurred at the same rate with diffe rent current injections. The voltage difference from the nadir to thre shold for the low-threshold calcium current, I-H, determined the inter burst interval. In contrast, with I-H present, the rate of depolarizat ion depended on injected current. With the full model, simulated repet itive cortical synaptic input entrained oscillations up to approximate ly double the natural frequency. Cortical input readily produced phase resetting as well. Our findings suggest that neither ascending brains tem control altering underlying hyperpolarization, nor descending driv e by repetitive cortical inputs, would alone be sufficient to produce the range of oscillation frequencies seen in thalamocortical neurons. Instead, intrinsic neuronal mechanisms would dominate for generating t he delta range (0.5-4 Hz) oscillations seen during slow wave sleep, wh ereas synaptic interactions with cortex and the thalamic reticular nuc leus would be required for faster oscillations in the frequency range of spindling (7-14 Hz).