1. The aim of this study was to document the kinematics and the electromyographic activity recorded from several muscles during treadmill locomotion in the same cat (N = 4), before and after spinalization by using a chronic implantation method. Because identical experimental and control conditions were used, it was possible to establish similarities and differences in the timing and amplitude of the muscular activity and kinematics under the intact and spinal conditions in the same animal. The data presented in this paper were collected when the cats had fully recuperated a stable locomotor pattern, walking at a constant speed of approximately 0.4 m/s. 2. The adult spinal cats retained many of the general locomotor features and electromyographic (EMG) characteristics seen before transection. However, there were also important differences. 3. There was a reduction in the step length that was principally due to the forward placement of the paw at the onset of the stance. Similarly, there was a decrease in the step cycle duration which was attributed to a reduction of both the stance and swing phases. 4. The overall angular excursions of the hip, knee, and ankle were generally similar, although joints were sometimes more flexed at all phases of the step cycle. In contrast, the overall excursions of the metatarsophalangeal joints was much greater in all four cats after spinalization due to a paw drag during the initial portion of the swing phase that exaggerated the plantarflexion. 5. There was an increase in the EMG amplitude of the flexor muscles at two of three joints (i.e., hip, knee, and ankle) in each cat after spinalization. The change in the EMG amplitude of the extensors did not appear to be as consistent as that observed in the flexor muscles. When looking at each cat individually, the postspinalization extensor activity decreased at two of three joints in two cats, whereas the opposite was true for the other two cats. 6. There was a delay in the onset of the knee flexor (semitendinosus) activity while the ankle dorsiflexor (tibialis anterior) activity started earlier with respect to the beginning of the swing phase. The onset of hip flexors was somewhat more variable. This change in the timing of flexor activity was most probably responsible for the paw drag at the onset of the swing phase. 7. The present results reveal that despite the few differences, the spinal cord and the hindlimbs afferents are capable of generating very good locomotor patterns with almost normal kinematics and EMG characteristics.

The re-expression of hindlimb locomotion after complete spinal cord injuries (SCIs) is caused by the presence of a spinal central pattern generator (CPG) for locomotion. After partial SCI, however, the role of this spinal CPG in the recovery of hindlimb locomotion in the cat remains mostly unknown. In the present work, we devised a dual-lesion paradigm to determine its possible contribution after partial SCI. After a partial section of the left thoracic segment T10 or T11, cats gradually recovered voluntary quadrupedal locomotion. Then, a complete transection was performed two to three segments more caudally (T13-L1) several weeks after the first partial lesion. Cats that received intensive treadmill training after the partial lesion expressed bilateral hindlimb locomotion within hours of the complete lesion. Untrained cats however showed asymmetrical hindlimb locomotion with the limb on the side of the partial lesion walking well before the other hindlimb. Thus, the complete spinalization revealed that the spinal CPG underwent plastic changes after the partial lesions, which were shaped by locomotor training. Over time, with further treadmill training, the asymmetry disappeared and a bilateral locomotion was reinstated. Therefore, although remnant intact descending pathways must contribute to voluntary goal-oriented locomotion after partial SCI, the recovery and re-expression of the hindlimb locomotor pattern mostly results from intrinsic changes below the lesion in the CPG and afferent inputs.

Traumatic lesions of the spinal cord yield a loss of supraspinal control of voluntary locomotor activity, although the spinal cord contains the necessary circuitry to generate the basic locomotor pattern. In spinal rats, this network, known as central pattern generator (CPG), was shown to be sensitive to serotonergic pharmacological stimulation. In previous works we have shown that embryonic raphe cells transplanted into the sublesional cord of adult rats can reinnervate specific targets, restore the lesion-induced increase in receptor densities of neurotransmitters, promote hindlimb weight support, and trigger a locomotor activity on a treadmill without any other pharmacological treatment or training.With the aim of discriminating whether the action of serotonin on CPG is associated to a specific level of the cord, we have transplanted embryonic raphe cells at two different levels of the sublesional cord (T9 and T11) and then performed analysis of the kinematic and EMG activity synchronously recorded during locomotion. Locomotor performances were correlated to the reinnervated level of the cord and compared to that of intact and transected nontransplanted animals. The movements expressed by T11 transplanted animals correspond to a well defined locomotor pattern comparable to that of the intact animals. On the contrary, T9 transplanted animals developed limited and disorganized movements as those of nontransplanted animals. The correlation of the locomotor performances with the level of reinnervation of the spinal cord suggests that serotonergic reinnervation of the L1-L2 level constitutes a key element in the genesis of this locomotor rhythmic activity. This is the firstin vivodemonstration that transplanted embryonic raphe cells reinnervating a specific level of the cord activate a locomotor behavior.

The recovery of voluntary quadrupedal locomotion after an incomplete spinal cord injury can involve different levels of the CNS, including the spinal locomotor circuitry. The latter conclusion was reached using a dual spinal lesion paradigm in which a low thoracic partial spinal lesion is followed, several weeks later, by a complete spinal transection (i.e., spinalization). In this dual spinal lesion paradigm, cats can express hindlimb walking 1 day after spinalization, a process that normally takes several weeks, suggesting that the locomotor circuitry within the lumbosacral spinal cord had been modified after the partial lesion. Here we detail the evolution of the kinematic locomotor pattern throughout the dual spinal lesion paradigm in five cats to gain further insight into putative neurophysiological mechanisms involved in locomotor recovery after a partial spinal lesion. All cats recovered voluntary quadrupedal locomotion with treadmill training (3-5 days/wk) over several weeks. After the partial lesion, the locomotor pattern was characterized by several left/right asymmetries in various kinematic parameters, such as homolateral and homologous interlimb coupling, cycle duration, and swing/stance durations. When no further locomotor improvement was observed, cats were spinalized. After spinalization, the hindlimb locomotor pattern rapidly reappeared, but left/right asymmetries in swing/stance durations observed after the partial lesion could disappear or reverse. It is concluded that, after a partial spinal lesion, the hindlimb locomotor pattern was actively maintained by new dynamic interactions between spinal and supraspinal levels but also by intrinsic changes within the spinal cord.

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