Abstract
BackgroundPeripheral tissue inflammation initiates hyperalgesia accompanied by tissue acidosis, nociceptor activation, and inflammation mediators. Recent studies have suggested a significantly increased expression of acid-sensing ion channel 3 (ASIC3) in both carrageenan- and complete Freund's adjuvant (CFA)-induced inflammation. This study tested the hypothesis that acupuncture is curative for mechanical hyperalgesia induced by peripheral inflammation.MethodsHere we used mechanical stimuli to assess behavioral responses in paw and muscle inflammation induced by carrageenan or CFA. We also used immunohistochemistry staining and western blot methodology to evaluate the expression of ASIC3 in dorsal root ganglion (DRG) neurons.ResultsIn comparison with the control, the inflammation group showed significant mechanical hyperalgesia with both intraplantar carrageenan and CFA-induced inflammation. Interestingly, both carrageenan- and CFA-induced hyperalgesia were accompanied by ASIC3 up-regulation in DRG neurons. Furthermore, electroacupuncture (EA) at the ST36 rescued mechanical hyperalgesia through down-regulation of ASIC3 overexpression in both carrageenan- and CFA-induced inflammation.ConclusionsIn addition, electrical stimulation at the ST36 acupoint can relieve mechanical hyperalgesia by attenuating ASIC3 overexpression.
Highlights
Peripheral tissue inflammation initiates hyperalgesia accompanied by tissue acidosis, nociceptor activation, and inflammation mediators
3.1 Carrageenan- and complete Freund’s adjuvant (CFA)-induced inflammatory hyperalgesia was attenuated using 2 Hz low frequency EA at the ST36 acupoint To test the mechanical hyperalgesia in inflammation pain, the mechanical stimuli were examined in both ipsilateral and contralateral paws
When the mice received the EA treatment, mechanical hyperalgesia attenuated at day 7 after intraplantar carrageenan injection (Figure 1b, 1.1 ± 0.4, open square, n = 8)
Summary
Peripheral tissue inflammation initiates hyperalgesia accompanied by tissue acidosis, nociceptor activation, and inflammation mediators. Tissue injury always results in inflammation that is often accompanied by sensitization of nerve terminal nociceptors innervating into the injury site. It is often initiated by a complex signaling to activate a complex response which alters the excitability of sensory neurons [3,4]. An animal model of inflammation pain was induced by injection of carrageenan or CFA into the peripheral tissue to induce both primary and secondary hyperalgesia [6,7]. Inflammation can sensitize nerve nociceptors both in peripheral and central nerve systems This can enhance neuronal excitability and increase responses to mechanical stimuli following inflammation [10,11]. Dorsal root ganglion (DRG), the spinal cord dorsal horn (SCDH), and brain neurons show increased nociceptive receptors and a decreased threshold to noxious stimulation during inflammation [12]
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