Central sensitization, caused either by tissue
inflammation or
peripheral nerve injury, plays an important role in persistent
pain. An animal model of
capsaicin-induced
pain has well-defined peripheral and central sensitization components, thus is useful for studying the
analgesic effect on two separate components. The focus of this study is to examine the
analgesic effects of
electroacupuncture (EA) on
capsaicin-induced secondary
hyperalgesia, which represents central sensitization.
Capsaicin (0.1%, 20 microl) was injected into the plantar side of the left hind paw, and foot withdrawal thresholds in response to von Frey stimuli (mechanical sensitivity) were determined for both primary and secondary
hyperalgesia in rats. EA (2 Hz, 3 mA) was applied to various pairs of
acupoints, GB30-GB34, BL40-BL60, GV2-GV6, LI3-LI6 and SI3-TE8, for 30 min under
isoflurane anesthesia and then the effect of EA on mechanical sensitivity of paw was determined. EA applied to the ipsilateral SI3-TE8, but to none of the other
acupoints, significantly reduced
capsaicin-induced secondary
hyperalgesia but not primary
hyperalgesia. EA
analgesic effect was inhibited by a systemic non-specific
opioid receptor (OR) antagonist or an intrathecal mu- or delta-OR antagonist. EA
analgesic effect was not affected by an intrathecal kappa-OR antagonist or systemic
adrenergic receptor antagonist. This study demonstrates that EA produces a stimulation point-specific
analgesic effect on
capsaicin-induced secondary
hyperalgesia (central sensitization), mediated by activating endogenous spinal mu- and
delta-opioid receptors.