“…The effects of training or clonidine observed in this study can then be attributed to changes occurring in spinal pathways and not to an alteration in peripheral sensory events or muscle fibers. There is now growing evidence that reflex pathways are not "hard-wired" (Forssberg and Svartengren, 1983), and that they can display a certain level of plasticity in response to central or peripheral lesions or operant conditioning (Mendell, 1984;Durkovic, 1996;Wolpaw, 1997;Wolpaw and Tennissen, 2001). The recovery of stepping with treadmill training has been attributed solely to plasticity of the CPG (Lovely et al, 1986;Rossignol, 1996;Harkema, 2001).…”
Treadmill training and clonidine, an ␣-2 noradrenergic agonist, have been shown to improve locomotion after spinal cord injury. We speculate that transmission in load pathways, which are involved in body support during stance, is specifically modified by training. This was evaluated by comparing two groups of spinal cats; one group (n ϭ 11) was trained to walk until full-weight-bearing (3-4 weeks), and the other (shams; n ϭ 7) was not. During an acute experiment, changes in group I pathways, monosynaptic excitation, disynaptic inhibition, and polysynaptic excitation were investigated by measuring the response amplitude in extensor motoneurons before and after clonidine injection. Monosynaptic excitation was not modified by clonidine but was decreased significantly by training. Disynaptic inhibition was significantly decreased by clonidine in both groups, but more significantly in trained cats, and significantly reduced by training after clonidine. Also, clonidine could reverse group IB inhibition into polysynaptic excitation in both groups but more frequently in trained cats. We also investigated whether fictive stepping revealed additional changes. In trained cats, the phase-dependent modulation of all three responses was similar to patterns reported previously, but in shams, modulation of monosynaptic and polysynaptic responses was not. Overall, training appears to decrease monosynaptic excitation and enhance the effects of clonidine in the reduction of disynaptic inhibition and reversal to polysynaptic excitation. Because it is believed that polysynaptic excitatory group I pathways transmit locomotor drive to extensor motoneurons, we suggest that the latter changes would facilitate the recruitment of extensor muscles for recovering weight-bearing during stepping.
“…The effects of training or clonidine observed in this study can then be attributed to changes occurring in spinal pathways and not to an alteration in peripheral sensory events or muscle fibers. There is now growing evidence that reflex pathways are not "hard-wired" (Forssberg and Svartengren, 1983), and that they can display a certain level of plasticity in response to central or peripheral lesions or operant conditioning (Mendell, 1984;Durkovic, 1996;Wolpaw, 1997;Wolpaw and Tennissen, 2001). The recovery of stepping with treadmill training has been attributed solely to plasticity of the CPG (Lovely et al, 1986;Rossignol, 1996;Harkema, 2001).…”
Treadmill training and clonidine, an ␣-2 noradrenergic agonist, have been shown to improve locomotion after spinal cord injury. We speculate that transmission in load pathways, which are involved in body support during stance, is specifically modified by training. This was evaluated by comparing two groups of spinal cats; one group (n ϭ 11) was trained to walk until full-weight-bearing (3-4 weeks), and the other (shams; n ϭ 7) was not. During an acute experiment, changes in group I pathways, monosynaptic excitation, disynaptic inhibition, and polysynaptic excitation were investigated by measuring the response amplitude in extensor motoneurons before and after clonidine injection. Monosynaptic excitation was not modified by clonidine but was decreased significantly by training. Disynaptic inhibition was significantly decreased by clonidine in both groups, but more significantly in trained cats, and significantly reduced by training after clonidine. Also, clonidine could reverse group IB inhibition into polysynaptic excitation in both groups but more frequently in trained cats. We also investigated whether fictive stepping revealed additional changes. In trained cats, the phase-dependent modulation of all three responses was similar to patterns reported previously, but in shams, modulation of monosynaptic and polysynaptic responses was not. Overall, training appears to decrease monosynaptic excitation and enhance the effects of clonidine in the reduction of disynaptic inhibition and reversal to polysynaptic excitation. Because it is believed that polysynaptic excitatory group I pathways transmit locomotor drive to extensor motoneurons, we suggest that the latter changes would facilitate the recruitment of extensor muscles for recovering weight-bearing during stepping.
“…For example, experiments in newts have shown that transplantations of flexors and exten sors, or the implantation of inverted supernumary limbs do not alter the pattern, even if this pattern is entirely contra productive [7]. Similar experiments with trans plantation of antagonist muscles in cats [8,9] and rats [10,114,115], have confirmed this lack of adaptability of the locomotor pattern. Why is it that the system here seems so rigidly captured in a certain pattern and how is this pattern generated?…”
In the last years it has become possible to regain some locomotor activity in patients suffering from an incomplete spinal cord injury (SCI) through intense training on a treadmill. The ideas behind this approach owe much to insights derived from animal studies. Many studies showed that cats with complete spinal cord transection can recover locomotor function. These observations were at the basis of the concept of the central pattern generator (CPG) located at spinal level. The evidence for such a spinal CPG in cats and primates (including man) is reviewed in part 1, with special emphasis on some very recent developments which support the view that there is a human spinal CPG for locomotion.
“…Comparisons of locomotor muscle activation patterns pre-and post-muscle transplantation surgery has found both relatively unchanged activations in children with cerebral palsy (Perry and Hoffer 1977;Waters et al 1982) and substantial modifications in patients with poliomyelitis (Close and Todd 1959;Sutherland et al 1960). Evidence from controlled animal studies found the original locomotor electromyography (EMG) patterns persisted following nerve crossing or muscle transpositions surgeries (Forssberg and Svartengren 1983;Sperry 1945). Cumulatively, this research suggests that there may be limitations of the motor system to adapt to either significant gain or connection changes in the neuromuscular map.…”
Gordon KE, Kinnaird CR, Ferris DP. Locomotor adaptation to a soleus EMG-controlled antagonistic exoskeleton. J Neurophysiol 109: 1804-1814, 2013. First published January 9, 2013 doi:10.1152/jn.01128.2011Locomotor adaptation in humans is not well understood. To provide insight into the neural reorganization that occurs following a significant disruption to one's learned neuromuscular map relating a given motor command to its resulting muscular action, we tied the mechanical action of a robotic exoskeleton to the electromyography (EMG) profile of the soleus muscle during walking. The powered exoskeleton produced an ankle dorsiflexion torque proportional to soleus muscle recruitment thus limiting the soleus' plantar flexion torque capability. We hypothesized that neurologically intact subjects would alter muscle activation patterns in response to the antagonistic exoskeleton by decreasing soleus recruitment. Subjects practiced walking with the exoskeleton for two 30-min sessions. The initial response to the perturbation was to "fight" the resistive exoskeleton by increasing soleus activation. By the end of training, subjects had significantly reduced soleus recruitment resulting in a gait pattern with almost no ankle push-off. In addition, there was a trend for subjects to reduce gastrocnemius recruitment in proportion to the soleus even though only the soleus EMG was used to control the exoskeleton. The results from this study demonstrate the ability of the nervous system to recalibrate locomotor output in response to substantial changes in the mechanical output of the soleus muscle and associated sensory feedback. This study provides further evidence that the human locomotor system of intact individuals is highly flexible and able to adapt to achieve effective locomotion in response to a broad range of neuromuscular perturbations.
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