Corticomotoneuronal cells contribute to long‐latency stretch reflexes in the rhesus monkey.

Abstract

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...

Coherence Between Motor Cortical Activity and Peripheral Discontinuities During Slow Finger Movements

“…It is known that cells in M1-including identified PTNs and CM cells-receive powerful input from the periphery. This comes both via S1 and also directly from the thalamus (Cheney and Fetz 1984;Lemon and Porter 1976;Rosen and Asanuma 1972). Muscle spindle afferent discharges are modulated by the movement discontinuities (Tracey et al 1980).…”

Voluntary reaction time and long-latency reflex modulation

“…When the participant is instructed to "resist" or "compensate" for the perturbation, M2 increases in magnitude and is followed a voluntary response; when the participant is told to "not intervene" or "let go," M2 is smaller in comparison (e.g., Calancie and Bawa 1985;Colebatch et al 1979;Hammond 1956;MacKinnon et al 2000).…”

“…One view attributes the amplitude modulation to be the result of an increase in the excitability of the reflex pathways (Calancie and Bawa 1985;Colebatch et al 1979;Hammond 1956; Lee and Tatton 1978;Pruszynski et al 2008;Selen et al 2012;Yang et al 2011). The opposing view suggests that the amplitude modulation is an artifact of the superposition of the voluntary response onto the end of the long-latency response (Crago et al 1976;Houk 1978; Lewis et al 2006;Manning et al 2012;Ravichandran et al 2013;Rothwell et al 1980).…”

Neuronal responses to tactile stimuli and tactile sensations evoked by microstimulation in the human thalamic principal somatic sensory nucleus (ventral caudal)

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