Intrathecal noradrenaline facilitates and inhibits the flexor reflex mediated by group II afferent fibers via alpha 1- and alpha 2-receptors, respectively.

The effects of intrathecal noradrenaline (NA) on the flexor reflex mediated by group II afferent fibers (group II flexor reflex) were investigated in anesthetized spinal rats. Low doses (0.01 and 0.1 mumol) of NA-HCl inhibited the group II flexor reflex, while high doses (1 and 10 mumol) facilitated it. In rats pretreated with the selective alpha 2-antagonist yohimbine-HCl (0.1 mumol), the effect of NA-HCl (0.1 mumol) shifted from inhibition to facilitation. Intravenous administration of prazosin-HCl (0.1 and 1 mg/kg, i.v.), a selective alpha 1-antagonist, dose-dependently antagonized the facilitation of the group II flexor reflex induced by NA-HCl in rats pretreated with yohimbine-HCl. The selective alpha 1-agonist methoxamine-HCl (1 mumol) and the alpha 2-agonist clonidine-HCl (0.1 mumol) facilitated and inhibited the group II flexor reflex, respectively. The effects of clonidine-HCl and methoxamine-HCl were almost the same as those of NA-HCl at doses of 0.1 and 10 mumol, respectively. NA-HCl (1 and 10 mumol) and methoxamine-HCl (1 mumol) increased the spontaneous electromyogram (EMG) spikes of the muscle tibialis anterior. The time course of the increase in the spontaneous EMG spikes was similar to that observed in the group II flexor reflex. These results suggest that NA facilitates and inhibits the group II flexor reflex via alpha 1- and alpha 2-receptors, respectively, and one of the mechanisms of the facilitatory effects is the elevation of excitability of the alpha-motoneuron.