Parametric studies on electroacupuncture-like stimulation in a rat model: effects of intensity, frequency, and...

We have found that electroacupuncture-like stimulation of defined sites in the hindlimb of the rat inhibits a nociceptive withdrawal reflex. The lightly anaesthetized rat was used and tall withdrawal from a noxious radiant heat stimulus was the nociceptive reflex. Standard stimulation of hindlimb meridian points femur-futu (ST-32), fengshi (GB-31), and zusanli (ST-36) consisted of a 2-ms square voltage pulse at 4 Hz for a duration of 20 min, applied at 20 times the threshold to evoke muscle twitch. This produced two types of inhibition of the reflex; one was an increase in the latency of up to 80% during the stimulation, termed the brief antinociception, and the other was a post stimulation increase of up to 60% lasting greater than 1 h, termed the persistent antinociception. When the stimulus intensity was reduced to 10 times threshold, the latency during stimulation increased up to 50%, but the persistent response did not occur. Stimulation at threshold produced neither effect. When the train duration was altered, 10 min of stimulation produced only the brief effect, whereas 40 min of stimulation produced both effects, although the persistent effect lasted only 20 min. Stimulation at 6 Hz produced responses similar to those at 4 Hz, whereas stimulation at 2 Hz produced smaller effects. At 8 Hz, only the brief antinociception was elicited. With a pulse duration of 0.2 ms, the brief response was observed but the persistent response was markedly attenuated, whereas 5 ms produced responses similar to those with 2 ms. These data suggest that high-intensity, low-frequency electrical stimulation of meridian points in the rat hindlimb produces both brief and persistent antinociceptive effects on the tail withdrawal reflex, and both effects are dependent upon the parameters of stimulation. The persistence of the latter effect beyond the period of stimulation suggests events occurring after direct synaptic activity, possibly mediated via plastic changes at spinal and/or supraspinal levels.