Loss of spinal mu-opioid receptor is associated with mechanical allodynia in a rat model of peripheral neuropathy.
The present study investigated whether the loss of spinal mu-opioid receptors following peripheral nerve injury is related to mechanical allodynia. We compared the quantity of spinal mu-opioid receptor and the effect of its antagonists, such as naloxone and CTOP, on pain behaviors in two groups of rats that showed extremely different severity of mechanical allodynia 2 weeks following partial injury of tail-innervating nerves. One group (allodynic group) exhibited robust signs of mechanical allodynia after the nerve injury, whereas the other group (non-allodynic group) showed little allodynia despite having suffered the same nerve injury. In addition, we investigated the quantity of spinal mu-opioid receptor and the effect of its antagonists on pain behaviors after the rats had recovered from mechanical allodynia 16 weeks following nerve injury. Immunohistochemical and Western blot analyses at 2 weeks after nerve injury indicated that spinal mu-opioid receptor content was more reduced in the allodynic group compared to the non-allodynic group. Intraperitoneal naloxone (2 mg/kg, i.p.) and intrathecal CTOP (10 microg/rat, i.t.) administration dramatically induced mechanical allodynia in the non-allodynic group. However, as in naïve animals, neither the loss of spinal mu-opioid receptors nor antagonist-induced mechanical allodynia was observed in the rats that had recovered from mechanical allodynia. These results suggest that the loss of spinal mu-opioid receptors following peripheral nerve injury is related to mechanical allodynia.
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Seung Keun
SK
Medical Science Research Center and Department of Physiology, Korea University College of Medicine, 126-1 Anam-dong 5 Ga, Seongbuk-Ku, Seoul 136-705, Republic of Korea.
Lee
Jaehee
J
Hong
Seung Kil
SK
Na
Heung Sik
HS
D000595:Amino Acid Sequence; D000818:Animals; D019771:Axotomy; D004195:Disease Models, Animal; D006930:Hyperalgesia / Q000209:etiology / Q000503:physiopathology*; D007274:Injections, Intraperitoneal; D007278:Injections, Spinal; D008297:Male; D008969:Molecular Sequence Data; D009270:Naloxone / Q000008:administration & dosage / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D009437:Neuralgia / Q000209:etiology / Q000503:physiopathology*; D020671:Posterior Horn Cells / Q000503:physiopathology; D011312:Pressure / Q000009:adverse effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D017450:Receptors, Opioid, mu / Q000187:drug effects / Q000502:physiology*; D013004:Somatostatin / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000494:pharmacology; D013116:Spinal Cord / Q000503:physiopathology*; D013127:Spinal Nerves / Q000293:injuries / Q000503:physiopathology*; D013314:Stress, Mechanical; D013623:Tail / Q000294:innervation
D009292:Narcotic Antagonists; C485765:Oprm1 protein, rat; D017450:Receptors, Opioid, mu; C049352:phenylalanyl-cyclo(cysteinyltyrosyl-tryptophyl-ornithyl-threonyl-penicillamine)threoninamide; D009270:Naloxone; D013004:Somatostatin