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The Journal of Neuroscience, August 27, 2003, 23(21):7950-7957

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Roles of ₁- and ₂-Adrenoceptors in the Nucleus Raphe Magnus in Opioid Analgesia and Opioid Abstinence-Induced Hyperalgesia

B. Bie,¹ H. L. Fields,² J. T. Williams,³ and Z. Z. Pan¹

¹Departments of Symptom Research and Biochemistry and Molecular Biology, University of Texas-M. D. Anderson Cancer Center, Houston, Texas 77030, ²Departments of Neurology and Physiology and the Wheeler Center for the Neurobiology of Addiction, University of California San Francisco, San Francisco, California 94143, and ³Vollum Institute, Oregon Health Sciences University, Portland, Oregon 97201

Noradrenaline and -adrenoceptors have been implicated in the modulation of pain in various behavioral conditions. Noradrenergic neurons and synaptic inputs are present in neuronal circuits critical for pain modulation, but their actions on neurons in those circuits and consequently the mechanisms underlying noradrenergic modulation of pain remain unclear. In this study, both recordings in vitro and behavioral analyses in vivo were used to examine cellular and behavioral actions mediated by ₁- and ₂-adrenoceptors on neurons in the nucleus raphe magnus. We found that ₁- and ₂-receptors were colocalized in the majority of a class of neurons (primary cells) that inhibit spinal pain transmission and are excited during opioid analgesia. Activation of the ₁-receptor depolarized whereas ₂-receptor activation hyperpolarized these neurons through a decrease and an increase, respectively, in potassium conductance. Blockade of the excitatory ₁-receptor or activation of the inhibitory ₂-receptor significantly attenuated the analgesia induced by local opioid application, suggesting that ₁-receptor-mediated synaptic inputs in these primary cells contribute to their excitation during opioid analgesia. In the other cell class (secondary cells) that is thought to facilitate spinal nociception and is inhibited by analgesic opioids, only ₁-receptors were present. Blocking the ₁-receptor in these cells significantly reduced the hyperalgesia (increased pain) induced by opioid abstinence. Thus, state-dependent activation of ₁-mediated synaptic inputs onto functionally distinct populations of medullary pain-modulating neurons contributes to opioid-induced analgesia and opioid withdrawal-induced hyperalgesia.

Key words: ₁-adrenoceptors; ₂-adrenoceptors; opioid; analgesia; hyperalgesia; pain; nucleus raphe magnus

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Received April 16, 2003; revised June 25, 2003; accepted July 3, 2003.

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