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.
View Article and Find Full Text PDFSevere traumatic lesions of the spinal cord yield a permanent deficit of motricity in adult mammals and specifically a loss of locomotor activity of hindlimbs when the lesion is located at the lower thoracic level. To restore this function, we have developed a paradigm of transplantation in rats based on a transection model of the spinal cord and the subsequent injection at the sublesional level of a suspension of embryonic brainstem monoaminergic neurons which play a key role in the modulation of locomotion. A genuine locomotion was characterized in transplanted animals by electromyographic and electroneurographic recordings.
View Article and Find Full Text PDFJ Neurosci Res
January 1999
The biogenic amine serotonin has been described in the literature as a powerful modulator of the spinal central pattern generator for locomotion. In the present study, we tested whether administration of serotonin or its agonist quipazine could restore motor activity in a model of paraplegia. One to three weeks after a complete transection of the spinal cord at a low thoracic level, rats were given either intrathecal injections of serotonin (5 mM, 15 microL) or intraperitoneal injections of quipazine (400-600 microg/kg).
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