INTENSE PERIPHERAL ELECTRICAL-STIMULATION DIFFERENTIALLY INHIBITS TAIL VS LIMB WITHDRAWAL REFLEXES IN THE RAT

In an on-going study on mechanisms by which activation of sensory affe rents regulates nociception, high-intensity, low-frequency electrical stimulation was applied to previously defined meridian and non-meridia n points of the hindlimb or forelimb, and the effects measured on the withdrawal reflex of the tail or limb in the lightly anesthetized rat. Withdrawal was evoked by application of noxious radiant heat to the t ip of the tail or to the plantar surface of a hindpaw or forepaw. Para meters of conditioning electrical stimulation were 2 ms pulses at 4 Hz for 20 min at 20 X threshold(20-30 mA) where threshold was the minimu m intensity which evoked muscle twitch. In experiments on tail withdra wal, stimulation applied to meridian points fengshi (GB-31), femur-fut u (ST-32) and zusanli (ST-36) of the hindlimb or to wai-kuan (TH-5) an d hoku (LI-4) of the forelimb increased the latency of the withdrawal reflex to 70-100% of the maximum possible inhibition (MPI) during the stimulation. Inhibition persisted for more than 1 h after the end of s timulation. Bilateral stimulation of hindlimb meridian points evoked a greater inhibition during the stimulation (> 95% of the MPI); the inh ibition persisted for 40 min. Stimulation of non-meridian sites in hin dlimb or forelimb inhibited the withdrawal reflexes by 45-50% of the M PI during the stimulation only. Thus, the evoked inhibition has two co mponents, a brief effect elicited by non-meridian point stimulation an d a persistent post-stimulation effect produced only upon stimulation of meridian points. Stimulation produced little effect on nociceptive limb withdrawal reflexes. The results suggest that high-intensity, low -frequency electrical stimulation of meridian points produced a long-l asting, extrasegmental inhibition of the tail withdrawal but not of li mb withdrawal reflexes. This differential inhibition may be due to dif ferences in neuronal circuitry and CNS modulatory control mechanisms. The persistent inhibition appears to be dependent on the site of stimu lation because it is not evoked by stimulation of sites outside of mer idian points.