EFFECTS OF ACTH ON PAIN RESPONSIVENESS IN MICE: INTERACTION WITH MORPHINE

SummaryPIntravenous (i.v.) injections of ACTH either enhanced (12.5 pg/kg) or slightly, though not significantly, suppressed (200 pg/kg) jumping in a modified hot plate test (46”C, 5 min exposure) in mice. Similarly, injections of morphine (0.037-0.156 mg/kg) markedly enhanced jumping whereas larger doses (0625-lO.Omg/kg) produced profound analgesia in this test. When administered simultaneously by a single intravenous injection, a larger dose of ACTH (200pg/kg) blocked the hyperalgesic effect of the small dose of morphine (i.e. 0.037 mg/kg). A small dose of ACTH (12.5 pg/kg), which by itself produced significant hyperalgesia, prevented the analgesic action of morphine (0.625 mg/kg). Taken together, the data suggest hat ACTH influences behaviourally-activated pain-controlling systems, possibly by inter-acting with opiate mechanisms in the brain. The ability of ACTH to alter the pharmacological actions of morphine as evident from the present results may be indicative of a requisite physiological function of ACTH in modulating the activity of endogenous opioids. Fragments of the polypeptide hormone, adrenocorti-cotropin (ACTH), appear to exert two diametrically opposite effects on pain responsiveness when adminis-tered centrally in rats. Intraventricular administratio