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PAIN MEDICINE

Differential Opioid Inhibition of C- and A- Fiber Mediated Thermonociception After Stimulation of the Nucleus Raphe Magnus

Ying Lu, MD^*, Sarah M. Sweitzer, PhD, Charles E. Laurito, MD^*, and David C. Yeomans, PhD

*Department of Anesthesiology, University of Illinois at Chicago, Chicago, Illinois, and the Department of Anesthesia, Stanford University School of Medicine, Stanford, California

Address correspondence and reprint requests to David C. Yeomans, PhD, Department of Anesthesia, Stanford University, 300 Pasteur Drive, S268, Stanford, CA 94305–5117. Address email to dcyeomans{at}stanford.edu

Although the importance of the nucleus raphe magnus in descending inhibitory control of nociception is clear, it is not known whether these effects are equivalent for different types of nociception. Thus, we examined the differential inhibition of behavioral responses evoked by A or C fiber thermonociceptor activation by electrical stimulation of nucleus raphe magnus neurons as well as the involvement of different classes of opiate receptors in this inhibition. In general, it was necessary to apply twice as much current to the nucleus raphe magnus to produce criterion antinociception for A mediated versus C fiber mediated nociceptive responses. Intrathecal administration of the nonselective opioid receptor antagonist, naltrexone, or the ₁ opioid receptor antagonist, naltrindole, attenuated both A and C fiber antinociception induced by nucleus raphe magnus stimulation with similar efficacy. In contrast, intrathecal administration of naloxonazine, a µ specific opioid receptor antagonist, or naltriben, a ₂ specific opioid receptor antagonist, preferentially attenuated nucleus raphe magnus induced antinociception for C fiber responses when compared with A mediated responses. These findings suggest that nociception evoked by the activation of A or C fiber nociceptors is under pharmacologically distinguishable descending control from the nucleus raphe magnus.

IMPLICATIONS: Opiates differentially inhibit pain produced by the activation of myelinated or unmyelinated pain sensing neurons, a distinction that is clinically important. This article demonstrates that the brain’s own pain control system operates with similar selectivity, and that this selectivity is partly mediated by different opiate receptor subtypes.

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