Interleukin 2-induced antinociception partially coupled with mu receptor.
The present study was designed to investigate the involvement of mu receptor in interleukin 2-induced antinociception. Intraplantar injection of human recombinant interleukin 2 (rIL-2) (1. 5x10(4) U) significantly enhanced pain threshold as measured by paw withdrawal latencies (PWLs) to noxious radiant heat in normal rats. After administration of rIL-2, PWLs were also markedly increased in morphine-tolerant and chronic constriction injury (CCI)-operated rats, which have been proven morphine-insensitive. rIL-2-induced antinociception in both morphine-tolerant and CCI-operated rats was significantly lower than that in normal rats. rIL-2 antinociception was partially blocked by naloxone (1 mg/kg i.p.) in normal rats but remained unchanged in the CCI group. Our results suggest that the use of rIL-2 in human medical practice may be extended for its effectiveness in relief of neuropathic pain induced by CCI. Here we infer that mu receptor plays an critical role in IL-2-induced antinociception and that there are also some other receptors involved in this process.
Key Laboratory of Neurobiology, Shanghai Institute of Physiology, Chinese Academy of Sciences, 320 Yue-Yang Road, Shanghai, 200031, P. R. China.
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D000700:Analgesics / Q000494:pharmacology; D000818:Animals; D006801:Humans; D007376:Interleukin-2 / Q000502:physiology*; D008297:Male; D010146:Pain; D010147:Pain Measurement; D051381:Rats; D017207:Rats, Sprague-Dawley; D017450:Receptors, Opioid, mu / Q000502:physiology*; D011994:Recombinant Proteins / Q000494:pharmacology
D000700:Analgesics; D007376:Interleukin-2; D017450:Receptors, Opioid, mu; D011994:Recombinant Proteins