Modeling corticothalamic feedback and the gating of the thalamus by the
cerebral cortex.
Alain Destexhe
Journal of Physiology (Paris) 94: 391-410, 2000.
Abstract
Morphological studies have shown that excitatory synapses from the cortex
constitute the major source of synapses in the thalamus. However, the effect
of these corticothalamic synapses on the function of the thalamus is not well
understood because thalamic neurones have complex intrinsic firing properties
and interact through multiple types of synaptic receptors. Here we investigate
these interactions using computational models. We show first, using models of
reconstructed thalamic relay neurones, that the effect of corticothalamic
synapses on relay cells can be similar to that of afferent synapses, in
amplitude, kinetics and timing, although these synapses are located in
different regions of the dendrites. This suggests that cortical EPSPs may
complement (or predict) the afferent information. Second, using models of
reconstructed thalamic reticular neurones, we show that high densities of the
low-threshold Ca2+ current in dendrites can give these cells an exquisite
sensitivity to cortical EPSPs, but only if their dendrites are hyperpolarized.
This property has consequences at the level of thalamic circuits, where
corticothalamic EPSPs evoke bursts in reticular neurones and recruit relay
cells predominantly through feedforward inhibition. On the other hand, with
depolarized dendrites, thalamic reticular neurones do not generate bursts and
the cortical influence on relay cells is mostly excitatory. Models therefore
suggest that the cortical influence can either promote or antagonize the relay
of information, depending on the state of the dendrites of reticular neurones.
The control of these dendrites may therefore be a determinant of attentional
mechanisms. We also review the effect of corticothalamic feedback at the
network level, and show how the cortical control over the thalamus is
essential in co-ordinating widespread, coherent oscillations. We suggest
mechanisms by which different modes of corticothalamic interaction would allow
oscillations of very different spatiotemporal coherence to coexist in the
thalamocortical system.
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