Effet de la buspirone sur le réflexe-H chez la souris adulte décérébrée spinale
Locomotion is generated by a spinal network which is, under normal conditions, modulated by supraspinal inputs and peripheral feedback. A spinal cord injury induces a loss of descending command and silence the locomotor network. Nevertheless, reexpression of this network can be facilitated by application of serotonin, a neurotransmitter originating supraspinally known to help locomotor recovery in spinal rodents. Such effect is associated with neuronal rearrangement which could be observed on reflex pathway. The aim of our study is to measure reflex modulation induced by buspirone, a 5-HT1A partial agonist that allowed reexpression of locomotion in adult spinal mice. Using a newly developed model of decerebrated unanesthetized mouse we measure the modulation of H-reflex excitability induced by buspirone after an acute spinal transection for 60 minutes post-injection. Comparison between buspirone (8mg/kg) treated (N=8) and control (N=6) groups present a significant decrease in reflex amplitude (69%) at early stages of pharmacological treatment followed by a raise (170%) that become significant 30 minutes postdose. Those results allowed us to associate reflexe decrease during prolocomotor period observed in first minutes after buspirone injection. There also support the involvement of buspirone in sensorimotor control.
serotonin motor function recovery reflex control monosynaptic reflex