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The Journal of Neurophysiology Vol. 83 No. 1 January 2000, pp. 99-115
Copyright ©2000 by the American Physiological Society
Department of Molecular and Integrative Physiology and Smith Mental Retardation and Human Development Research Center, University of Kansas Medical Center, Kansas City, Kansas 66160
McKiernan, Brian J.,
Joanne K. Marcario,
Jennifer Hill Karrer, and
Paul D. Cheney.
Correlations Between Corticomotoneuronal (CM) Cell Postspike
Effects and Cell-Target Muscle Covariation. J. Neurophysiol. 83: 99-115, 2000. The presence of postspike
facilitation (PSpF) in spike-triggered averages of electromyographic
(EMG) activity provides a useful means of identifying cortical neurons
with excitatory synaptic linkages to motoneurons. Similarly the
presence of postspike suppression (PSpS) suggests the presence of
underlying inhibitory synaptic linkages. The question we have addressed
in this study concerns the extent to which the presence and strength of
PSpF and PSpS from corticomotoneuronal (CM) cells correlates with the
magnitude of covariation in activity of the CM cell and its target
muscles. For this purpose, we have isolated cells during a reach and
prehension task during which the activity of 24 individual proximal and
distal forelimb muscles was recorded. These muscles show broad
coactivation but with a highly fractionated and muscle specific fine
structure of peaks and valleys. Covariation was assessed by computing
long-term (2 s) cross-correlations between CM cells and forelimb
muscles. The magnitude of cross-correlations was greater for muscles
with facilitation effects than muscles lacking effects in
spike-triggered averages. The results also demonstrate a significant
relationship between the sign of the postspike effect (facilitation or
suppression) and the presence of a peak or trough in the
cross-correlation. Of all the target muscles with facilitation effects
in spike-triggered averages (PSpF, PSpF with synchrony, or synchrony
facilitation alone), 89.5% were associated with significant
cross-correlation peaks, indicating positively covarying muscle and CM
cell activity. Seven percent of facilitation effects were not
associated with a significant effect in the cross-correlation, whereas
only 3.4% of effects were associated with correlation troughs. In
contrast, of all the muscles with suppression effects in
spike-triggered averages, 38.9% were associated with significant
troughs in the cross-correlation, indicating an inverse relation
between CM cell and muscle activity consistent with the presence of
suppression. Fifty-five percent of suppression effects was associated
with correlation peaks, whereas 5.6% was not associated with a
significant effect in the cross-correlation. Limiting the analysis to
moderate and strong facilitation effects, the magnitude of PSpF was
correlated weakly with the magnitude of the cell-muscle
cross-correlation peak. Nevertheless, the results show that although
many CM cell-target muscle pairs covary during the reach and prehension
task in a way consistent with the sign and strength of the CM cell's
synaptic effects on target motoneurons, many exceptions exist. The
results are compatible with a model in which control of particular
motoneuron pools reflects not only the summation of signals from many
CM cells but also signals from additional descending, sensory afferent, and intrinsic spinal cord neurons. Any one neuron will make only a
small contribution to the overall activity of the motoneuron pool. In
view of this, it is not surprising that relationships between postspike
effects and CM cell-target muscle covariation are relatively weak with
many apparent incongruities.
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