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The rostral ventromedial medulla (RVM), or ventromedial nucleus of the spinal cord, is a group of neurons located close to the midline on the floor of the medulla oblongata (myelencephalon). The rostral ventromedial medulla sends descending inhibitory and excitatory fibers to the dorsal horn spinal cord neurons. There are 3 categories of neurons in the RVM. On-cells, off-cells, and neutral cells. They are characterized by their response to nociceptive input. Off-cells show a transitory decrease in firing rate right before a nociceptive reflex, and are theorized to be inhibitory.〔 Activation of off-cells, either by morphine or by any other means, results in antinociception. On-cells show a burst of activity immediately preceding nociceptive input, and are theorized to be contributing to the excitatory drive. Neutral cells show no response to nociceptive input.〔 == Involvement in Neuropathic pain == Research has shown the RVM to be important in the maintenance of neuropathic pain. Ablation of μ-opioid-expressing neurons in the RVM with a dermorphin-saporin conjugate eliminated the allodynia and hyperalgesia caused by a nerve injury. Treatment with the dermorphin-saporin conjugate did not alter baseline pain thresholds, or affect sensitivity in the first 5–10 days after nerve injury. This suggests that the RVM contributes to the persistent pathology caused by nerve injury. Further research determined that a large majority of μ-opioid-expressing neurons also expressed CCK2 receptors. Microinjection in the RVM with either a CCK-saporin or a dermorphin-saporin conjugate eliminated neurons expressing either receptor. Injection of the CCK-saporin conjugate also reversed allodynia and hyperalgesia in a nerve injury model, producing the same results as the dermorphin-saporin conjugate. This destruction of neurons was relatively specific, as less than 10% of neurons in the RVM were destroyed. This suggests that the targeted neurons are the ones responsible for maintaining chronic neuropathic pain states, and that the observed effect was not due to diffuse destruction of RVM neurons. In addition, lidocaine microinjections into the RVM temporarily reversed allodynia and hyperalgesia caused by nerve injury.〔 To help determine whether the persistent pain state was centrally or peripherally mediated, non-noxious stimuli were applied to the nerve-injured limb. In animals receiving vehicle injections into the RVM, there was an increase in FOS expression in the superficial and deep dorsal horn of the spinal cord, indicating activation of nociceptive neurons. Animals receiving the dermorphin-saporin conjugate into the RVM had significantly less FOS expression. This indicates that a persistent neuropathic pain state is centrally mediated.〔 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「rostral ventromedial medulla」の詳細全文を読む スポンサード リンク
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