The physiological function of the descending noradrenergic system in the spinal ventral horn has not yet been fully elucidated. Here we describe our recent findings showing the motor function of the noradrenergic fibers. 1) α1-Antagonists and α2-agonists depressed the spinal mono and polysynaptic reflex potentials in rats that have an intact connection between the spinal cord and the brain. In rats spinalized at the Cl level, the α1-agonistic action of adrenergic agents increased the spinal reflexes. 2) In the radio frequency-lesioned decerebrate rigidity model of rats, α1-antagonists and α2-agonists reduced the rigidity by affecting the spinal and supraspinal levels, respectively. 3) α2-Agonists but not α1-antagonists reduced noradrenaline released into the subarachnoid space of anesthetized rats. 4) In a slice preparation isolated from adult rats, the α1-agonistic action of adrenergic agents increased the excitatory synaptic transmission of the ventral horn. Thus, it was demonstrated that α2-agonistic action at the brain stem inhibited spinal motor activity by reducing the release of noradrenaline in the spinal cord, and that the facilitatory action through α1-adrenoceptors was dominant in descending noradrenergic transmission in the motor nuclei of the ventral horn.