Abstract
Intraperitoneally applied ACTH produced either hyperalgesia or analgesia depending upon dose; 60 μg/kg ACTH produced hyperalgesia, and 250 μg/kg ACTH produced analgesia. Analgesia was abolished by hypophy-sectomy or mesencephalic lesion leaving the hyperalgesia unchanged. Maximum hyperalgesia was produced by 0.6 μg/rat intrathecal ACTH. The maximum was reached in 30 minutes, and then reduced to the control level 75 minutes after application. The effect was competitively antagonized by intraperitoneal 0.6 mg/kg dexamethasone. It was strongly suggested that hyperalgesia might be produced by activation of ACTH sensitive sites in the spinal cord, and analgesia might be produced by such sites at the supraspinal level.
