Pain transmission in the spinal dorsal horn (SDH) is regulated by descending neuronal pathways from the brain, such as noradrenergic (NAergic) neurons from the locus coeruleus. While it is known that spinal NA produces an antinociceptive effect, we have recently shown that NA has an ability to produce pain hypersensitivity via Hes5-expressing SDH astrocytes. However, the mechanism underlying the bidirectional effect of spinal NA remains unknown. In this study, we showed that while intrathecal injection of NA at a low dose (NA^low) induced pain hypersensitivity via α_1A-adrenergic receptors (α_1A-ARs) in Hes5⁺ astrocytes, the hypersensitivity was not observed by intrathecal high-dose NA (NA^high). The effect of NA^high was also mediated by activation of inhibitory interneurons via α_1A-ARs. We found that NA^high also activated β₁-ARs in astrocytes that suppressed the astrocytic α_1A-ARs-mediated effect. However, if α_1A-ARs are expressed in inhibitory interneurons, why does NA^low produce pain hypersensitivity? We further found that activation of astrocytic α_1A-ARs increased release of adenosine, a factor that suppresses inhibitory interneurons. Therefore, our findings indicate that NA bidirectionally modulates pain transmission via astrocyte-neuron interactions in a concentration-dependent manner.