In a previous study, the authors have suggested that there is a central mechanism in pain modulation of TENS, and interferential current therapy(ICT) by using the tail-flick reflex and measuring the cerebrospinal fluid Ղ-endorphin of the rat. To confirm this central opiate-mediated pain modulation, we examined the reversal of a delayed tail-flick reflex latency and the cerebrospinal fluid Ղ-endorphin level by the naloxone administration. We measured the latencies of fictive tail-flick reflex before, immediately after TENS, ICT, and 15 minutes after naloxone administration. Cerebrospinal fluid Ղ-endorphin was also measured quantitatively by radioimmunoassay after TENS, ICT and naloxone administration.

The results revealed that in the group with TENS application, the latency of tail flick reflex after naloxone administration(31.54⁑5.08) was reversed to the level before the TENS application(34.76⁑6.09 msec) compared to the level after the TENS application(were 42.28⁑10.14 msec). With ICT application, the latency of tail flick reflex after naloxone administration(32.46⁑5.52msec) was also reversed to the level before the ICT (33.39⁑4.72 msec) application compared to the level immediately after the ICT application(46.87⁑10.14 msec). The Ղ-endorphin levels in cerebrospinal fluid were significantly decreased in the groups of naloxone administration, both with the TENS(14.86⁑3.92 pmol/l) and the ICT applications(18.04⁑3.93 pmol/l) compared to the control group(52.05⁑14.12 pmol/l).

We confirmed that the central pain modulation mechanism of TENS and ICT was through the reversal of delayed tail-flick reflex latency and elevated CSF β-endorphin level after naloxone administration