Differential back-invasion of a single complex dendrite of an abducens motoneuron by N-methyl-D-aspartate-induced oscillations: a simulation study.
Intracellular recording of abducens motoneurons in vivo has shown that ionophoretic applications of N-methyl-D-aspartate produced long-lasting membrane potential oscillations including a slow depolarization plateau with a burst of fast action potentials. This complex N-methyl-D-aspartate pattern was reproduced in the model of abducens motoneuron in vivo identified, intracellularly stained with horseradish peroxidase and reconstructed at high spatial resolution. The excitable soma of the simulated cell contained voltage-gated Ca, Na and K conductances, N-methyl-D-aspartate-gated voltage-sensitive Ca-Na-K conductance and Ca-dependent K conductance. The dendrite was passive either completely or with the exception of branching nodes containing N-methyl-D-aspartate conductances of the same slow kinetics but of lower values than at the soma. In the completely passive case, the N-methyl-D-aspartate pattern decayed with different rates along different dendritic paths depending on the geometry and topology of the reconstructed dendrite. The branches formed four clusters discriminated in somatofugal attenuations of steady voltages, and were correspondingly discriminated in attenuation of the complex N-methyl-D-aspartate pattern. Fast spikes decayed more than the slow depolarization plateau so that the prevalence of slow over fast components in the transformed pattern increased with somatofugal path distance. As a consequence, the lower the electrotonic effectiveness of a branch in the cluster or in the whole arborization, the lower both the voltage level and the frequency range of its voltage modulation by N-methyl-D-aspartate oscillations. In the case of active branching points, the somatic pattern changed depending on the level of activation of dendritic N-methyl-D-aspartate conductances with slow kinetics of voltage sensitivity. The higher this level, the longer the plateau and burst, and the greater the discharge rate; and the spikes in the burst were smaller. When the pattern spread in the dendrite, the fast spikes decayed and the slow plateau was boosted, with a greater effect along the somatofugal path containing more branching points. These results show how the somatofugal back-invasion along the dendrites by activity patterns generated at the soma can tune voltage-sensitive dendritic conductances. The dendritic back-invasion is geometry- and topology-dependent. It is proposed as a subtle feedback mechanism for the neuron to control its own synaptic inputs.
Korogod
S M
SM
Research Laboratory of Biophysics and Bioelectronics, Dniepropetrovsk State University, Ukraine.
Kopysova
I L
IL
Bras
H
H
Gogan
P
P
Tyc-Dumont
S
S
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D003198:Computer Simulation; D003712:Dendrites / Q000187:drug effects / Q000502:physiology*; D015640:Ion Channel Gating; D007473:Ion Channels / Q000502:physiology; D008564:Membrane Potentials / Q000187:drug effects; D008959:Models, Neurological; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology*; D018482:Muscle, Skeletal / Q000294:innervation*; D016202:N-Methylaspartate / Q000494:pharmacology*; D009991:Oscillometry; D013997:Time Factors
D007473:Ion Channels; D016202:N-Methylaspartate