Functional linkages between motor cortical cells and elbow flexor muscles; Evidence for and characteristics of post-spike facilitation. Fourment, A., A. Belhaj-Sa[diaeresis]if and B. Maton. Laboratoire de Physiologie du Mouvement, ERS CNRS 102,Universit[acute]e Paris-Sud, F-91405 Orsay, France.
APStracts 2:0070N, 1995.
SUMMARY AND CONCLUSIONS
1. Two monkeys (Macaca fascicularis) making high-level but submaximal isometric flexions of the elbow, were investigated for the output effect of motor cortical cells upon the EMG activity of two main elbow flexors using the method of spike-triggered averaging of rectified EMGs (STAs). 2. Monkeys were trained to perform individual isometric contractions for longer than two seconds, and two series of at least 20 contractions, the second series being at a greater force. EMG electrodes pairs were implanted in the biceps brachii and brachioradialis. A total of 257 cortical cells were found that discharged with the active and passive movements of the elbow. We examined the EMG facilitatory effects (PSFs) produced in either one or the two flexors for only those cells which discharged during the isometric contraction, and provoked PSFs in the two series of contractions. 3. The main characteristics of the EMG isometric contractions in the agonists were analysed. Spectral analysis showed that the increases in the EMG median frequency with force stabilized at the force levels performed by monkeys. Cross-correlation methods showed no cross- talk between agonists. 4. The 26 selected cortical cells had a regular discharge frequency. Ten cells did not change frequency with a 22-30% force increase, 14 cells discharged at a higher frequency, and two cells at a lower frequency. For single cell frequencies of 5 - 65 Hz, interspike intervals shorter than 10 ms were rare: the median and modal intervals were 20 - 30 ms. 5. The significance of PSFs with respect to the EMG background noise was estimated statistically. STAs from successive epochs under identical load conditions, and STAs performed at a distance from the trigger showed that PSFs were authentic post-spike effects, and not sudden EMG changes synchronized by chance with the triggering cell. The features distinguishing PSF from secondary post-spike EMG changes or co-activation and task-related effects were studied in simultaneous STAs of flexors and autocorrelogram of cortical spikes. 6. The magnitude of the PSF was expressed as the percent peak amplitude above the mean EMG baseline. The mean percent amplitude of the 90 PSFs produced in both muscles and series was 4.0 +/- 2.4%. There was no difference in the average amplitude of PSFs in the two flexors, although the baseline voltages in the biceps brachii were higher. Neither was there any significant change with force while the baseline level increased by 29 +/- 10%, indicating that the absolute PSF amplitude increased in the same proportion as baseline. 7. The mean onset latency was 9.4 +/- 4.2 ms for all PSFs, but it was 6.9 +/- 1.8 ms for two thirds of the PSFs. The differences in flexors were not significant. There was a weak correlation between the PSF amplitudes and latencies. 8. Nineteen cells co-facilitated the two flexors. 15 cells facilitated the two flexors at the same latency within a 4 ms range at each force level, and 11 did it for the two levels of force. 9. We conclude that motor cortical cells exert an excitatory effect on elbow flexor muscles via monosynaptic or disynaptic linkages. 

Received 19 April 1994; accepted in final form 6 March 1995.
APS Manuscript Number J203-4.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on  3 April 1995.