Selective depression of medium‐latency leg and foot muscle responses to stretch by an alpha 2‐agonist in humans.

Corna, Stefano; Grasso, Margherita; Nardone, Antonio; Schieppati, Marco

doi:10.1113/jphysiol.1995.sp020705

Cited by 94 publications

(63 citation statements)

References 18 publications

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“…This might be related to the higher sensitivity of spinal group II inputs to neuromodulation by monoamines (midbrain structures relaying motor cortex outflow). Indeed, excitatory spinal group II inputs at cervical and lumbar levels have been particularly depressed by ␣ 2 -noradrenergic agonists, while group I inputs were unchanged (Corna et al 1995;Lourenço et al 2006;Marque et al 2004;Maupas et al 2004;Rémy-Néris et al 2003). Therefore, while group I and group II commissural interneurons can receive common descending inputs, it appears that the two subpopulations can be controlled differentially rather than being coactivated during voluntary movement, as suggested in cats (Jankowska et al 2005).…”

Section: Modulation During Motor Tasksmentioning

confidence: 99%

Task-related modulation of crossed spinal inhibition between human lower limbs

Hanna-Boutros

Sangari

Karasu

et al. 2014

Journal of Neurophysiology

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Hanna-Boutros B, Sangari S, Karasu A, Giboin LS, MarchandPauvert V. Task-related modulation of crossed spinal inhibition between human lower limbs. J Neurophysiol 111: 1865-1876, 2014. First published February 5, 2014 doi:10.1152/jn.00838.2013.-Crossed reflex action mediated by muscle spindle afferent inputs has recently been revealed in humans. This raised the question of whether a complex spinal network involving commissural interneurons receiving inputs from proprioceptors and suprasegmental structures, as described in cats, persists in humans and contributes to the interlimb coordination during movement. First, we investigated the neurophysiological mechanisms underlying crossed reflex action between ankle plantar flexors and its corticospinal control from primary motor cortex. Second, we studied its modulation during motor tasks. We observed crossed inhibition in contralateral soleus motoneurons occurring with about 3 ms central latency, which is consistent with spinal transmission through oligosynaptic pathway. The early phase of inhibition was evoked with lower stimulus intensity than the late phase, suggesting mediation by group I and group II afferents, respectively. The postsynaptic origin of crossed inhibition is confirmed by the finding that both H-reflex and motor-evoked potential were reduced upon conditioning stimulation. Transcranial magnetic stimulation over ipsilateral and contralateral primary motor cortex reduced crossed inhibition, especially its late group II part. Last, late group II crossed inhibition was particularly depressed during motor tasks, especially when soleus was activated during the walking stance phase. Our results suggest that both group I and group II commissural interneurons participate in crossed reflex actions between ankle plantar flexors. Neural transmission at this level is depressed by descending inputs activated by transcranial magnetic stimulation over the primary motor cortex or during movement. The specific modulation of group II crossed inhibition suggests control from monoaminergic midbrain structures and its role for interlimb coordination during locomotion.H-reflex; TMS; commissural interneurons; corticospinal; locomotion SEVERAL SPINAL PATHWAYS INVOLVING commissural interneurons mediate crossed reflex actions from proprioceptors. In cat lumbar cord, these pathways are closely interconnected and incorporated into complex networks coordinating muscle activity on both sides (Jankowska 2008).

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Section: Modulation During Motor Tasksmentioning

confidence: 99%

Task-related modulation of crossed spinal inhibition between human lower limbs

Hanna-Boutros

Sangari

Karasu

et al. 2014

Journal of Neurophysiology

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“…The red arrow indicates the location of the stimulation. applied to the Achilles' tendon using a vibratory stimulus of 70 Hz frequency and 1 mm amplitude; (2) frequency-dependent depression of proprioceptive reflexes was tested by delivering two successive pulses of EES at intervals of 50 and 100 ms ; and (3) pharmacological modulation of EES-evoked motor responses was tested using the ␣2-adrenergic receptor agonist Tizanidine (1 mg/kg), which decreases excitability of spinal interneurons supplied by Group II fibers (Corna et al, 1995), and the sodium channel blocker tetrodotoxin (TTX; concentration, 1 M; volume of bolus, 50 l), which suppresses synaptic transmission (Tresch and Kiehn, 2000). Both pharmacological agents were injected into the subarachnoid space of the spinal cord through an inlet cannula.…”

Section: Methodsmentioning

confidence: 99%

A Computational Model for Epidural Electrical Stimulation of Spinal Sensorimotor Circuits

et al. 2013

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Epidural electrical stimulation (EES) of lumbosacral segments can restore a range of movements after spinal cord injury. However, the mechanisms and neural structures through which EES facilitates movement execution remain unclear. Here, we designed a computational model and performed in vivo experiments to investigate the type of fibers, neurons, and circuits recruited in response to EES. We first developed a realistic finite element computer model of rat lumbosacral segments to identify the currents generated by EES. To evaluate the impact of these currents on sensorimotor circuits, we coupled this model with an anatomically realistic axon-cable model of motoneurons, interneurons, and myelinated afferent fibers for antagonistic ankle muscles. Comparisons between computer simulations and experiments revealed the ability of the model to predict EES-evoked motor responses over multiple intensities and locations. Analysis of the recruited neural structures revealed the lack of direct influence of EES on motoneurons and interneurons. Simulations and pharmacological experiments demonstrated that EES engages spinal circuits trans-synaptically through the recruitment of myelinated afferent fibers. The model also predicted the capacity of spatially distinct EES to modulate side-specific limb movements and, to a lesser extent, extension versus flexion. These predictions were confirmed during standing and walking enabled by EES in spinal rats. These combined results provide a mechanistic framework for the design of spinal neuroprosthetic systems to improve standing and walking after neurological disorders.

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“…Tizanidine, an α 2 adrenergic receptor agonist, selectively blocks transmission from group II afferents in the lumbar spinal cord both in the cat (Bras et al 1990) and in human subjects (Corna et al 1995;Marque et al 2005). Assuming that it would have similar actions on circuits of the cervical cord, the effects of ulnar nerve stimulation on the ongoing FCR EMG activity were investigated before and after oral intake of tizanidine.…”

Section: Group Datamentioning

confidence: 99%

“…Only recently has it become possible to investigate group II pathways in the lower limb of human subjects. Most of the group II effects described so far are superimposed on group I effects, so that special tests are required to differentiate their contributions: cooling the nerve (Matthews, 1989;Schieppati & Nardone, 1997;Simonetta-Moreau et al 1999) and depression of group II excitation by tizanidine, an α 2 adrenergic receptor agonist (Corna et al 1995;Marque et al 2005). These investigations have shown that group II excitation of motoneurones, whether homonymous or heteronymous (Simonetta-Moreau et al 1999;Marque et al 2005), is more potent than excitation by Ia afferents in corresponding pathways.…”

mentioning

confidence: 99%

Mediation of late excitation from human hand muscles via parallel group II spinal and group I transcortical pathways

Lourenço

Iglesias

Cavallari

et al. 2006

The Journal of Physiology

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This study addresses the question of the origin of the long-latency responses evoked in flexors in the forearm by afferents from human hand muscles. The effects of electrical stimuli to the ulnar nerve at wrist level were assessed in healthy subjects using post-stimulus time histograms for flexor digitorum superficialis and flexor carpi radialis (FCR) single motor units (eight subjects) and the modulation of the ongoing rectified FCR EMG (19 subjects). Ulnar stimulation evoked four successive peaks of heteronymous excitation that were not produced by purely cutaneous stimuli: a monosynaptic Ia excitation, a second group I excitation attributable to a propriospinally mediated effect, and two late peaks. The first long-latency excitation occurred 8-13 ms after monosynaptic latency and had a high-threshold (1.2-1.5 × motor threshold). When the conditioning stimulation was applied at a more distal site and when the ulnar nerve was cooled, the latency of this late excitation increased more than the latency of monosynaptic Ia excitation. This late response was not evoked in the contralateral FCR of one patient with bilateral corticospinal projections to FCR motoneurones. Finally, oral tizanidine suppressed the long-latency high-threshold excitation but not the early low-threshold group I responses. These results suggest that the late high-threshold response is mediated through a spinal pathway fed by muscle spindle group II afferents. The second long-latency excitation, less frequently observed (but probably underestimated), occurred 16-18 ms after monosynaptic latency, had a low threshold indicating a group I effect, and was not suppressed by tizanidine. It is suggested that this latest excitation involves a transcortical pathway.

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Selective depression of medium‐latency leg and foot muscle responses to stretch by an alpha 2‐agonist in humans.

Cited by 94 publications

References 18 publications

Task-related modulation of crossed spinal inhibition between human lower limbs

Task-related modulation of crossed spinal inhibition between human lower limbs

A Computational Model for Epidural Electrical Stimulation of Spinal Sensorimotor Circuits

Mediation of late excitation from human hand muscles via parallel group II spinal and group I transcortical pathways

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