Suppression of neuropathic pain by peripheral electrical stimulation in rats: μ-opioid receptor and NMDA receptor implicated

Sun, Ruixia; Wang, Hechun; Wan, You; Zheng, Jing; Luo, Fei; Han, Ji-Sheng; Wang, Yun

doi:10.1016/j.expneurol.2003.12.011

Cited by 40 publications

(18 citation statements)

References 35 publications

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“…Systemic administration of naloxone blocked 2 Hz electroacupuncture inhibition of L5 and L6 spinal nerve ligation (SNL)- and caudal trunk nerve injury-induced neuropathic pain. 130,131 Manual acupuncture, applied at ST36 and SP6 in an SNL-induced neuropathic pain rat model, significantly reduced SNL-induced hypersensitivity; this effect was blocked by systemic nolaxone. 132 Furthermore, administration of cumulative doses (5, 10, 20 nmol) of the μ or δ opioid receptor antagonists β-funaltrexamine hydrochloride and naltrindole blocked 2-Hz-produced electroacupuncture anti-mechanical allodynia, corroborating μ and δ opioid receptor involvement in electroacupuncture action.…”

Section: Neuropathic Pain Modelsmentioning

confidence: 93%

Mechanisms of Acupuncture–Electroacupuncture on Persistent Pain

Zhang

Lao

Ren³

et al. 2014

Anesthesiology

650

465

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In the last decade, preclinical investigations of electroacupuncture mechanisms on persistent tissue-injury (inflammatory), nerve-injury (neuropathic), cancer, and visceral pain have increased. These studies show that electroacupuncture activates the nervous system differently in health than in pain conditions, alleviates both sensory and affective inflammatory pain, and inhibits inflammatory and neuropathic pain more effectively at 2–10 Hz than at 100 Hz. Electroacupuncture blocks pain by activating a variety of bioactive chemicals through peripheral, spinal, and supraspinal mechanisms. These include opioids, which desensitize peripheral nociceptors and reduce pro-inflammatory cytokines peripherally and in the spinal cord, and serotonin and norepinephrine, which decrease spinal n-methyl-d-aspartate receptor subunit GluN1 phosphorylation. Additional studies suggest that electroacupuncture, when combined with low dosages of conventional analgesics, provides effective pain management that can forestall the side effects of often-debilitating pharmaceuticals.

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Section: Neuropathic Pain Modelsmentioning

confidence: 93%

Mechanisms of Acupuncture–Electroacupuncture on Persistent Pain

Zhang

Lao

Ren³

et al. 2014

Anesthesiology

650

465

View full text Add to dashboard Cite

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“…Mechanical sensitivity to punctate tactile stimuli was determined with use of calibrated von Frey filaments by using the up-and-down paradigm as in our previous study (Chaplan et al, 1994;Sun et al, 2004). The response to mechanical threshold was determined 30,60,90,120,150, and 180 min after injection.…”

Section: Pain Behavior Testingmentioning

confidence: 99%

CCL2 and CXCL1 trigger calcitonin gene-related peptide release by exciting primary nociceptive neurons

2005

Self Cite

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Chemokines are important mediators in immune responses and inflammatory processes. Calcitonin gene-related peptide (CGRP) is produced in dorsal root ganglion (DRG) neurons. In this study, CGRP radioimmunoassay was used to investigate whether the chemokines CCL2 and CXCL1 could trigger CGRP release from cultured DRG neurons of neonatal rats and, if so, which cellular signaling pathway was involved. The results showed that CCL2 and CXCL1 ( approximately 5-100 ng/ml) evoked CGRP release and intracellular calcium elevation in a pertussis toxin (PTX)-sensitive manner. The CGRP release by CCL2 and CXCL1 was significantly inhibited by EGTA, omega-conotoxin GVIA (an N-type calcium channel blocker), thapsigargin, and ryanodine. Pretreatment of DRG neurons for 30 min with the inhibitors of phospholipase C (PLC) and protein kinase C (PKC) but not mitogen-activated protein kinases (MAPKs) significantly reduced CCL2- or CXCL1-induced CGRP release and intracellular calcium elevation. Intraplantar injection of CCL2 or CXCL1 produced hyperalgesia to thermal and mechanical stimulation in rats. These data suggest that CCL2 and CXCL1 can stimulate CGRP release and intracellular calcium elevation in DRG neurons. PLC-, PKC-, and calcium-induced calcium release from ryanodine-sensitive calcium stores signaling pathways are involved in CCL2- and CXCL1-induced CGRP release from primary nociceptive neurons, in which chemokines produce painful effects via direct actions on chemokine receptors expressed by nociceptive neurons.

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“…They also found that acupuncture induces analgesia in the rat models for neuropathic [69][70][71] or inflammatory [72,73] pain. Nociceptin/orphanin FQ and its receptors in the spinal cord and brain stem were found to be involved in acupuncture analgesia in chronic pain models [74,75].…”

Section: Mechanisms For Acupuncture Analgesiamentioning

confidence: 92%

Pain research in China

Zhang

2010

Sci. China Life Sci.

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In addition to investigating the anatomy, neurochemistry and neurophysiology of pain pathways, Chinese researchers have extended their work into the molecular and cellular mechanisms of sensory afferent transmission at the spinal cord level as well as cognitive processing in the brain. The mechanism underlying acupuncture analgesia remains a subject of special interest for Chinese pain researchers, with the aim of combining clinical practice with the understanding of pain transmission and analgesic mechanism.

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Suppression of neuropathic pain by peripheral electrical stimulation in rats: μ-opioid receptor and NMDA receptor implicated

Cited by 40 publications

References 35 publications

Mechanisms of Acupuncture–Electroacupuncture on Persistent Pain

Mechanisms of Acupuncture–Electroacupuncture on Persistent Pain

CCL2 and CXCL1 trigger calcitonin gene-related peptide release by exciting primary nociceptive neurons

Pain research in China

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