Antinociceptive effect of peripheral segmental electrical stimulation in the rat.

We have investigated the effect of transcutaneous electrical stimulation, applied to the base of the tail, on the flexor withdrawal response of the rat, following immersion of the tail in water at 49 degrees C. In intact rats, electrical stimulation delayed the response to the controlled noxious stimulus, the delay depending on the duration of stimulation and on the frequency and pulse width of the stimulus. The prolongation in reaction time produced by stimulation at 100 Hz, 0.2 msec for 30 min at a voltage sufficient to cause slight fibrillation of the tail muscles, but no escape behaviour, was equal to that produced by 7.5 mg/kg of morphine. The specific narcotic antagonist naloxone (1 mg/kg) virtually abolished the effect of the electrical stimulation. After recovery from the operation, rats with complete spinal transection at the 10th or 11th thoracic vertebra exhibited a flexor withdrawal response to the noxious stimulus behaviourally simpler and of shorter latency than that exhibited by the intact animals. Peripheral electrical stimulation again delayed the response, and naloxone prevented the delay, but the antinociceptive action of the stimulation was quantitatively less than that observed in intact animals. Morphine also had a correspondingly reduced effect in the spinal animals. Depletion of 5-hydroxytryptamine levels by systemic pretreatment with parachlorphenylalanine significantly diminished the effect of both electrical stimulation and morphine administration in intact rats, but not in spinal rats. Our results support the concept that peripheral electrical stimulation excites naloxone-dependent antinociceptive mechanisms at both spinal and supraspinal levels. The supraspinal mechanism, but not the spinal mechanism, is associated with 5-hydroxytryptamine.