The strength, latency, and time course of most PSF suggest they are mediated by monosynaptic corticomotoneuronal (CM) connections, although a contribution through indirect linkages cannot be excluded. Taking the strong and moderate PSF as evidence of CM connections, the present results indicate that CM cells commonly distribute divergent terminals to motoneurons of more than one muscle. The larger muscle fields of extensor cells may reflect a greater divergence of terminals than flexor cells.

No abstract

The purpose of this study was to systematically map the forelimb area of primary motor cortex (M1) in rhesus macaques in an effort to investigate further the organization of motor output to distal and proximal muscles. We used stimulus-triggered averaging (StTAing) of electromyographic activity to map the cortical representation of 24 simultaneously recorded forelimb muscles. StTAs were obtained by applying 15 A stimuli to M1 sites while the monkey performed a reach and prehension task. Motor output to body regions other than the forelimb (e.g., face, trunk, and hindlimb) was identified using repetitive intracortical microstimulation to evoke movements. Detailed, muscle-based maps of M1 revealed a central core of distal (wrist, digit, and intrinsic hand) muscle representation surrounded by a "horseshoe"-shaped zone of proximal (shoulder and elbow) muscle representation. The core distal and proximal zones were separated by a relatively large region representing combinations of both distal and proximal muscles. On the basis of its size and characteristics, we argue that this zone is not simply the result of stimulus-current spread, but rather a distinct zone within the forelimb representation containing cells that specify functional synergies of distal and proximal muscles. Electrode tracks extending medially from the medial arm of the proximal muscle representation evoked trunk and hindlimb responses. No distal or proximal muscle poststimulus effects were found in this region. These results argue against the existence of a second, major noncontiguous distal or proximal forelimb representation located medially within the macaque M1 representation.

We used spike-triggered averaging of rectified electromyographic activity to determine whether corticomotoneuronal (CM) cells produce postspike effects in muscles of both proximal and distal forelimb joints in monkeys performing a reach and prehension task. Two monkeys were trained to perform a self-paced task in which they reached forward from a starting position to retrieve a food reward from a small cylindrical well. We compiled spike-triggered averages from 22 to 24 separate forelimb muscles at both proximal (shoulder, elbow) and distal (wrist, digits, intrinsic hand) joints. Of 174 cells examined, 112 produced postspike effects in at least one of the target muscles. Of those cells, 45.5% produced postspike effects in both proximal and distal forelimb muscles. A nearly equal number (44.7%) produced postspike effects in distal muscles only, whereas a clear minority (9.8%) produced postspike effects in only proximal muscles. The majority of CM cells (71.4%) produced effects in two or more muscles, with an average muscle field of 3.1 +/- 2.1 (mean +/- SD) for facilitation plus suppression. Of 345 postspike effects identified, 70.7% were facilitation effects and 29.3% were suppression effects. The large majority of effects (72.2%) were in distal muscles. When averaged by joint, the latency and peak magnitude of postspike facilitation showed a stepwise increase from proximal to distal joints. The results of this study show that the majority of CM cells engaged in coordinated forelimb reaching movements facilitate and/or suppress muscles at multiple joints, including muscles at both proximal and distal joints. The results also show that CM cells make more frequent and more potent terminations in motoneuron pools of distal compared with proximal muscles.

SUMMARY1. To test the hypothesis that a transcortical reflex contributes to the stretch-evoked long-latency electromyographic (e.m.g.) response we documented the responses of identified corticomotoneuronal (c.m.) cells and their target muscles to perturbations of active wrist movements. Macaque monkeys performed ramp-and-hold wrist movements against elastic loads, alternating between flexion and extension zones; brief (25 ms) torque pulses were intermittently applied during the hold period.2. C.m. cells were identified by a clear post-spike facilitation in spike-triggered averages of forelimb muscle e.m.g. activity. Activity of c.m. cells and twelve wrist and digit flexor and extensor muscles was recorded during: (a) active ramp-and-hold wrist movements, (b) passive ramp-and-hold wrist movements, and (c) torque perturbations applied during the hold phase of active flexion and extension which either lengthened or shortened the c.m. cell's target muscles.3. Muscle-lengthening perturbations evoked a reproducible pattern of average e.m.g. activity in the stretched muscles, consisting of two peaks: the first response (M1) had an onset latency of 1 -2+2-1 ms (mean+S.D.), and the second (M2) began at 27-9 +51 ms. Torque perturbations which shortened the active muscles also evoked a characteristic e.m.g. response consisting of an initial cessation of activity at 13-5 + 3-4 ms followed by a peak beginning at 33 9 + 3-0 ms.4. The responses of twenty-one c.m. cells which facilitated wrist muscles were documented with torque pulse perturbations applied during active muscle contraction. Twenty of twenty-one c.m. cells responded at short latency (23-4 ± 8-8 ms) to torque perturbations which stretched their target muscles.5. For each c.m. cell-target muscle pair, transcortical loop time was calculated as the sum of the onset latency of the c.m. cell's response to lengthening perturbations (afferent time) and the onset latency of post-spike facilitation (efferent time). The mean transcortical loop time was 304+ t10-2 ms, comparable to the mean onset latency of the M2 peak (27-9 + 5 1). The duration of a c.m. cell's response to torque perturbations provides a further measure of the extent of its potential contribution to the M2 muscle response. In all cases but two, the c.m. cell response, delayed by the latency of the post-spike facilitation, overlapped the M2 e.m.g. peak. P. D. CHENEY AND E. E. FETZ6. In addition to responding to perturbations which stretched their target muscles, as predicted by the transcortical stretch reflex hypothesis, eight of eighteen c.m. cells also responded at short latency (22-0 ± 7-4 ms) to perturbations which shortened their target muscles. These excitatory responses were appropriately timed to contribute to the long-latency e.m.g. peak in their target muscles evoked by muscle-shortening perturbations. The functional consequence of the long-latency coactivation of flexors and extensors is a stiffening of the joint, to which these bidirectionally activated c.m. cells contribute.7. Seventeen ofnine...