Backpropagation of the δ oscillation and the retinal excitatory postsynaptic potential in a multi-compartment model of thalamocortical neurons

Uniform and non-uniform somato-dendritic distributions of the ion channels carrying the low-threshold Ca 2+ current ( I T), the hyperpolarization-activated inward current ( I h), the fast Na + current ( I Na) and the delayed rectifier current ( I K) were investigated in a multi-compartment model of...

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Veröffentlicht in:Neuroscience 2000-01, Vol.98 (1), p.111-127
Hauptverfasser: Emri, Z, Antal, K, Tóth, T.I, Cope, D.W, Crunelli, V
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Sprache:eng
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Zusammenfassung:Uniform and non-uniform somato-dendritic distributions of the ion channels carrying the low-threshold Ca 2+ current ( I T), the hyperpolarization-activated inward current ( I h), the fast Na + current ( I Na) and the delayed rectifier current ( I K) were investigated in a multi-compartment model of a thalamocortical neuron for their suitability to reproduce the δ oscillation and the retinal excitatory post-synaptic potential recorded in vitro from the soma of thalamocortical neurons. The backpropagation of these simulated activities along the dendritic tree was also studied. A uniform somato-dendritic distribution of the maximal conductance of I T and I K ( g T and g K, respectively) was sufficient to simulate with acceptable accuracy: (i) the δ oscillation, and its phase resetting by somatically injected current pulses; as well as (ii) the retinal excitatory postsynaptic potential, and its α-amino-3-hydroxy-5-methyl-4-isoxazole proprionate and/or N-methyl- d-aspartate components. In addition, simulations where the dendritic g T and g K were either reduced (both by up to 34%) or increased (both by up to 15%) of their respective value on the soma still admitted a successful reproduction of the experimental activity. When the dendritic distributions were non-uniform, models where the proximal and distal dendritic g T was up to 1.8- and 1.2-fold larger, respectively, than g T(s) produced accurate simulations of the δ oscillation (and its phase resetting curves) as well as the synaptic potentials without need of a concomitant increase in proximal or distal dendritic g K. Furthermore, an increase in proximal dendritic g T and g K of up to fourfold their respective value on the soma resulted in acceptable simulation results. Addition of dendritic Na + channels to the uniformly or non-uniformly distributed somato-dendritic T-type Ca 2+ and K + channels did not further improve the overall qualitative and quantitative accuracy of the simulations, except for increasing the number of action potentials in bursts elicited by low-threshold Ca 2+ potentials. Dendritic I h failed to produce a marked effect on the simulated δ oscillation and the excitatory postsynaptic potential. In the presence of uniform and non-uniform dendritic g T and g K, the δ oscillation propagated from the soma to the distal dendrites with no change in frequency and voltage-dependence, though the dendritic action potential amplitude was gradually reduced towards the distal dendrites. The amplitude
ISSN:0306-4522
1873-7544
DOI:10.1016/S0306-4522(00)00068-3