Wei F, Zou S, Robbins MT, Ren K, Dubner R (2004) Mu-opioid receptor-expressing neurons in the nucleus reticularis gigantocellularis contribute to descending facilitation during the development of inflammatory pain. Neuroscience 2004 Abstracts 297.3. Society for Neuroscience, San Diego, CA.
Summary: We have previously shown that nucleus reticularis giangocellularis (NGC) is involved in descending facilitation of inflammatory hyperalgesia. The cellular mechanisms of descending facilitation from the NGC are unknown. The targeted destruction of the mu-opioid receptor-containing neurons in the rostral ventromedial medulla (RVM) by a dermorphin-saporin conjugate prevents nerve injury-induced hyperalgesia in rats (Porreca et al., J. Neurosci. 21:5281, 2001). We examined the effects of selective deletion of the mu-opioid receptor-expressing neurons in the sub-regions of RVM on nocifensive behaviors in rats. After microinjection of dermorphin-saporin conjugate (1.5 pmol/500 nl) into the RVM, there were no changes in baseline thermal and mechanical sensitivity to noxious stimuli. However, the injection of dermorphin-saporin conjugate into bilateral NGC (n=7) significantly attenuated the thermal hyperalgesia and mechanical allodynia at 30 min to 1 d after hindpaw inflammation produced by injection of complete Freund’s adjuvant, compared to sham (blank-saporin or dermorphin) groups (n=3-6). The lesion of the nucleus raphe magnus (NRM) (n=3) only slightly reduced hyperalgesia at 3 h after inflammation. The loss of NGC mu-opioid receptor-containing neurons also decreased nocifensive behaviors only in phase II of the formalin model. In contrast, NRM lesions were without an effect on formalin-induced phase I/II responses. These findings indicate that selective deletion of the mu-opioid receptor-containing neurons in the nucleus reticularis giangocellularis attenuates inflammatory hyperagesia and allodynia.
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