Experiments were conducted to test morphine sensitivity of the flexion reflex in the anemic decerebrate cats. Animals were immobilized with gallamine triethiodide(Flxaedil) and were artificially ventilated. The sural nerve was electrically stimulated(20V, 0.5 msec) and the flexion reflex was obtained by recording compound action potentials from the nerve innervated to the semitendinosus muscle. Intravenous injection of morphine (0.5~2.0 mg/kg) was found to have following effects on the flexion reflex. 1) Morphine tended to depress the early component of the flexion reflex and the effect was widely variable between animal preparations. 2) Morphine significantly depressed the late component of the flexion reflex, the effect being proportional to the dose of morphine. 3) The morphine effect on the flexion reflex was reversed by a small dose of naloxone hydrochloride(0.025~0.1 mg/kg). 4) Naloxone hydrochloride alone did not appear to facilitate the flexion reflex. 5) The main site for the morphine action was found to be the brain stem. From these results and those reported in literatures, we conclude that the late component of the flexion reflex well represents the pain sensation, thus the late component of the flexion reflex can be used as a reasonable subjective index of pain in experimental animals.