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).