title: The effects of opioid receptor antagonists on electroacupuncture-produced anti-allodynia/hyperalgesia in rats with paclitaxel-evoked peripheral neuropathy.
abstract: Research supports the effectiveness of acupuncture for conditions such as chronic low back and knee pain. In a five-patient pilot study the modality also improved the symptoms of chemotherapy-induced neuropathic pain. Using an established rat model of paclitaxel-induced peripheral neuropathy, we evaluated the effect of electroacupuncture (EA) on paclitaxel-induced hyperalgesia and allodynia that has not been studied in an animal model. We hypothesize that EA would relieve the paclitaxel-induced mechanical allodynia and hyperalgesia, which was assessed 30 min after EA using von Frey filaments. Beginning on day 13, the response frequency to von Frey filaments (4-15 g) was significantly increased in paclitaxel-injected rats compared to those injected with vehicle. EA at 10 Hz significantly (P<0.05) decreased response frequency at 4-15 g compared to sham EA; EA at 100 Hz only decreased response frequency at 15 g stimulation. Compared to sham EA plus vehicle, EA at 10 Hz plus either a μ, δ, or κ opioid receptor antagonist did not significantly decrease mechanical response frequency, indicating that all three antagonists blocked EA inhibition of allodynia and hyperalgesia. Since we previously demonstrated that μ and δ but not κ opioid receptors affect EA anti-hyperalgesia in an inflammatory pain model, these data show that EA inhibits pain through different opioid receptors under varying conditions. Our data indicate that EA at 10 Hz inhibits mechanical allodynia/hyperalgesia more potently than does EA at 100 Hz. Thus, EA significantly inhibits paclitaxel-induced allodynia/hyperalgesia through spinal opioid receptors, and EA may be a useful complementary treatment for neuropathic pain patients.
authors.affiliation: Center for Integrative Medicine, School of Medicine, University of Maryland, Baltimore, MD 21201, USA.
authors.forename: Xianze
authors.initials: X
authors.lastname: Meng
authors.forename: Yu
authors.initials: Y
authors.lastname: Zhang
authors.forename: Aihui
authors.initials: A
authors.lastname: Li
authors.forename: Jiajia
authors.initials: J
authors.lastname: Xin
authors.forename: Lixing
authors.initials: L
authors.lastname: Lao
authors.forename: Ke
authors.initials: K
authors.lastname: Ren
authors.forename: Brian M
authors.initials: BM
authors.lastname: Berman
authors.forename: Ming
authors.initials: M
authors.lastname: Tan
authors.forename: Rui-Xin
authors.initials: RX
authors.lastname: Zhang
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000972:Antineoplastic Agents, Phytogenic / Q000633:toxicity; D004195:Disease Models, Animal; D015671:Electroacupuncture / Q000379:methods*; D006930:Hyperalgesia / Q000503:physiopathology / Q000628:therapy*; D008297:Male; D009271:Naltrexone / Q000031:analogs & derivatives* / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology*; D017239:Paclitaxel / Q000633:toxicity; D010147:Pain Measurement; D017288:Pain Threshold / Q000187:drug effects* / Q000502:physiology; D010523:Peripheral Nervous System Diseases / Q000139:chemically induced / Q000628:therapy*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013004:Somatostatin / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D000972:Antineoplastic Agents, Phytogenic; D009292:Narcotic Antagonists; C049352:phenylalanyl-cyclo(cysteinyltyrosyl-tryptophyl-ornithyl-threonyl-penicillamine)threoninamide; C051844:norbinaltorphimine; D013004:Somatostatin; D009271:Naltrexone; C055382:naltrindole; D017239:Paclitaxel