Spinal cats on the treadmill: changes in load pathways.
Treadmill training and clonidine, an alpha-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 = 11) was trained to walk until full-weight-bearing (3-4 weeks), and the other (shams; n = 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.
Côté
Marie-Pascale
MP
Centre de Recherche en Sciences Neurologiques, Département de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Québec, Canada H3C 3J7.
Ménard
Ariane
A
Gossard
Jean-Pierre
JP
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000344:Afferent Pathways; D000818:Animals; D002415:Cats; D003000:Clonidine / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects; D005080:Exercise Test; D005260:Female; D008124:Locomotion; D009046:Motor Neurons / Q000502:physiology*; D018482:Muscle, Skeletal / Q000294:innervation; D009433:Neural Inhibition; D009473:Neuronal Plasticity; D011434:Proprioception; D012018:Reflex; D013116:Spinal Cord / Q000502:physiology* / Q000601:surgery; D013119:Spinal Cord Injuries / Q000628:therapy; D009435:Synaptic Transmission; D013904:Thoracic Vertebrae / Q000601:surgery; D016474:Weight-Bearing
D000316:Adrenergic alpha-Agonists; D003000:Clonidine