Patterns of facilitation and suppression of antagonist forelimb muscles from motor cortex sites in the awake monkey

Patterns of excitatory and inhibitory effects were produced in antagonistic forelimb muscles by single intracortical microstimuli (S-ICMS) applied to motor cortex sites in macaque monkeys performing ramp-and-hold wrist movements. Stimulus-triggered averages (stimulus-TAs) of rectified electromyographic (EMG) activity revealed poststimulus facilitation and/or suppression in identified flexor and extensor muscles of the wrist and fingers. At 22 cortical sites the action potentials of single cells were also recorded and used to compute spike-triggered averages (spike-TAs) of covarying muscles. The set of muscles activated during the movement in which the cell was active are referred to here as "agonists"; those muscles active during wrist movement in the opposite direction are called "antagonists." (At sites where cells were not isolated the muscles showing poststimulus facilitation were called agonists.) Poststimulus effects in agonist muscles typically consisted of facilitation in a subset of the agonists. For 48 sites from which poststimulus effects were tested on both flexors and extensors, the following combinations of effects were observed: 1) pure facilitation of agonist muscles with no effect on antagonists; 2) facilitation of both agonists and antagonists; 3) facilitation of agonist muscles with reciprocal suppression of antagonists; 4) "mixed" facilitation and suppression of synergist muscles; and 5) pure suppression of some muscles with no effect on their antagonists. The suppression effects appeared most commonly in flexor muscles; conversely, facilitation was generally stronger in extensors. Cortical sites eliciting pure suppression of flexor muscles with no facilitation of extensor muscles were found in two monkeys. These purely suppressive effects were observed not only in stimulus-TAs but also in spike-TAs computed from single cells at these sites. Some of these cells increased their activity during wrist extension (but had no detectable effect on the extensor muscles); others discharged during flexion. Several observations suggest that the cortically evoked suppression is mediated by polysynaptic relays. The mean onset latency of the postspike suppression (7.4 ms) produced by inhibitory cells was longer than the mean onset latency of postspike facilitation (6.7 ms) produced by CM cells. Similarly, the mean onset latency of poststimulus suppression (8.9 ms) was longer than that of poststimulus facilitation (8.0 ms). Moreover, suppression was usually weaker than facilitation in the spike-TAs, as well as in stimulus-TAs compiled for the same stimulus intensity.(ABSTRACT TRUNCATED AT 400 WORDS)