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Journal of Neurophysiology, Vol 60, Issue 1 60-85, Copyright © 1988 by APS
ARTICLES |
J. W. Fleshman, I. Segev and R. B. Burke
Laboratory of Neural Control, National Institute of Neurological and Communicative Disorders and Stroke, Bethesda, Maryland 20892.
1. Measurements of input resistance (RN), time constant (tau 0), and electrotonic length (Lpeel) were derived from intracellular voltage changes produced by injection of current pulses in six type-identified triceps surae alpha-motoneurons. The motoneurons were labeled with horseradish peroxidase and subsequently reconstructed and measured from serial sections. These quantitative morphological and physiological data were incorporated into detailed computer models of the motoneurons. 2. Steady-state and dynamic models were used to determine values for specific membrane resistivity (Rm) that matched the experimental estimates of RN, tau 0, and Lpeel for each motoneurons. The models were based on the following assumptions 1) the membrane was electrically passive, 2) cytoplasmic resistivity (Ri) was 70 omega-cm, and 3) "sealed-end" boundary conditions were present at dendritic terminations. We also considered the nature and magnitude of possible errors introduced by using linear (passive) computer models to match responses from motoneurons with nonlinear (i.e., voltage-dependent) conductances. 3. If we assume that the experimental measurements of RN and tau 0 were correct, uniform Rm values that reproduced the experimentally measured RN required widely varying values of Cm (1.4-8.6 microF/cm2) to match the experimental tau 0. Furthermore, the electrotonic distance to dendritic terminals was generally much greater than expected from physiological estimates of Lpeel. However, if we assumed that the RN measurements could have been underestimated by as much as 30% and that Cm = 1.0 microF/cm2, it was possible to choose spatially uniform Rm that matched the observed tau 0 in three of six cases. 4. Relaxing the assumption of spatially uniform membrane resistivity permitted us to reconcile the anatomical and physiological characteristics of all six motoneurons. Two qualitatively different models of Rm nonuniformity gave equally good fits to the experimental results 1) a step-wise increase in Rm from a low value at the soma to a much higher but uniform value over the entire dendritic tree, and 2) a monotonic increase in Rm from soma to distal dendrites as a sigmoidal function of path distance along the dendrites. The step and sigmoidal models of the spatial distribution of Rm generated different electrotonic architectures in motoneuron dendritic trees, but both gave essentially identical electrical responses at the soma.(ABSTRACT TRUNCATED AT 400 WORDS)
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