Transmission within several spinal pathways in adults with cerebral palsy.

Many studies have investigated the changes of spinal neuronal networks in patients with cortico-subcortical or spinal lesions occurring during adulthood. In contrast, little is known about modifications of transmission within spinal networks implied in motor control for patients suffering from perinatal lesions. In the present series of experiments, we have investigated, in adult patients with cerebral palsy who suffered cerebral damage in the perinatal period, the efficacy of transmission within four spinal networks known for exhibiting pathophysiological changes following a central nervous system lesion occurring in adulthood. These are presynaptic Ia inhibition, post-activation depression, disynaptic reciprocal Ia inhibition and propriospinally-mediated Group I and Group II facilitations. In 28 patients with cerebral palsy and 35 age-matched healthy subjects we were able to show that: (i) disynaptic reciprocal Ia inhibition is intact in patients with cerebral palsy; (ii) both presynaptic Ia inhibition and post-activation depression are impaired in patients with cerebral palsy; and (iii) propriospinally-mediated Group I facilitation is undamaged in patients with cerebral palsy, whereas Group II facilitation is strongly enhanced. Only diminished post-activation depression was highly correlated to the severity of spasticity. Differences in the spinal transmission between patients with cerebral palsy and patients who suffered neuronal damage in adulthood are discussed.

Modulation of recurrent inhibition from knee extensors to ankle motoneurones during human walking.

The neural control for muscle coordination during human locomotion involves spinal and supraspinal networks, but little is known about the exact mechanisms implicated. The present study focused on modulation of heteronymous recurrent inhibition from knee extensors to ankle motoneurones at different times in the gait cycle, when quadriceps (Quad) muscle activity overlaps that in tibialis anterior (TA) and soleus (Sol). The effects of femoral nerve stimulation on ankle motoneurones were investigated during treadmill walking and during tonic co-contraction of Quad and TA/Sol while standing. Recurrent inhibition of TA motoneurones depended on the level of background EMG, and was similar during walking and standing for matched background EMG levels. On the other hand, recurrent inhibition in Sol was reduced in early stance, with respect to standing, and enhanced in late stance. Reduced inhibition in Sol was also observed when Quad was coactivated with TA around the time of heel contact, compared to standing at matched background EMG levels in the two muscles. The modulation of recurrent inhibition of Sol during walking might reflect central and/or peripheral control of the Renshaw cells. These modulations could be implicated in the transition phases, from swing to stance to assist Sol activation during the stance phase, and from stance to swing, for its deactivation.

[The PAI-1 swing: microenvironment and cancer cell migration]. / Microenvironnement cellulaire, PAI-1 et migration cancéreuse.

Cancer is a complex and dynamic process caused by a cellular dysfunction leading to a whole organ or even organism vital perturbation. To better understand this process, we need to study each one of the levels involved, which allows the scale change, and to integrate this knowledge. A matricellular protein, PAI-1, is able to induce in vitro cell behaviour modifications, morphological changes, and to promote cell migration. PAI-1 influences the mesenchymo-amaeboid transition. This matricellular protein should be considered as a potential 'launcher' of the metastatic process acting at the molecular, cellular, tissular levels and, as a consequence, at the organism's level.