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Vol. 289, Issue 2, 840-846, May 1999
Physical Therapy Graduate Program (M.D., A.S., S.S., A.T.) and
Neuroscience Graduate Program (K.A.S.), The University of Iowa,
Iowa City, Iowa
Transcutaneous electrical nerve stimulation (TENS) is commonly used for
relief of pain. The literature on the clinical application of TENS is
extensive. However, surprisingly few reports have addressed the
neurophysiological basis for the actions of TENS. The gate control
theory of pain is typically used to explain the actions of
high-frequency TENS, whereas, low-frequency TENS is typically explained
by release of endogenous opioids. The current study investigated the
role of µ,
, and
opioid receptors in antihyperalgesia produced
by low- and high-frequency TENS by using an animal model of
inflammation. Antagonists to µ (naloxone),
(naltrinodole), or
(nor-binaltorphimine) opioid receptors were delivered to the spinal
cord by microdialysis. Joint inflammation was induced by injection of
kaolin and carrageenan into the knee-joint cavity. Withdrawal latency
to heat was assessed before inflammation, during inflammation, after
drug (or artificial cerebral spinal fluid as a control) administration,
and after drug (or artificial cerebral spinal fluid) administration + TENS. Either high- (100 Hz) or low- frequency (4 Hz) TENS
produced approximately 100% inhibition of hyperalgesia. Low doses of
naloxone, selective for µ opioid receptors, blocked the
antihyperalgesia produced by low-frequency TENS. High doses of
naloxone, which also block
and
opioid receptors, prevented the
antihyperalgesia produced by high-frequency TENS. Spinal blockade of
opioid receptors dose-dependently prevented the antihyperalgesia
produced by high-frequency TENS. In contrast, blockade of
opioid
receptors had no effect on the antihyperalgesia produced by either low-
or high-frequency TENS. Thus, low-frequency TENS produces
antihyperalgesia through µ opioid receptors and high-frequency TENS
produces antihyperalgesia through
opioid receptors in the spinal cord.
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