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一氧化氮 (NO)近来被认为是神经系统执行各种信息传递任务的气体性递质或调质 ,现已知NO易化脊髓水平痛觉的传递。我们推测 ,在此处 ,NO可能也参与痛觉的脑干下行性抑制系统。本实验用脚掌注射福尔马林引起同侧脊髓腰膨大背角神经元伤害性c fos表达 ,结合鞘内注射一氧化氮合成酶抑制剂的方法 ,来观察NO是否参与脊髓背角神经元痛反应以及对于该反应的下行抑制活动。第一部分实验表明 ,一侧脚掌注射福尔马林可引起同侧脊髓腰膨大背角神经元伤害性c fos表达 ;鞘内注射一氧化氮合成酶抑制剂左旋硝基精氨酸L NNA可剂量依赖性地抑制其表达。在第二部分实验中 ,先对大鼠实施了脊髓胸段背半部单侧离断手术 ,然后双侧脚掌注射福尔马林 ,此时可见完好侧脊髓背角c fos表达数量明显少于损伤侧。这种差异只能解释为完好侧保存着由脑干发出、下行投射到脊髓腰膨大的痛觉抑制系统抑制了该侧背角c fos表达的结果 ;进一步实验证明 ,这种抑制作用可以被鞘内注射L NNA取消。这个结果表明 :NO不仅易化脊髓水平伤害性信号的传递活动 ,同时也增强痛觉的下行性抑制系统的作用。
Nitric oxide (NO) has recently been identified as a potent neurotransmitter or regulator of various informational tasks in the nervous system. It is now known that nociception of nociception at the level of the NO-facilitated spinal cord is known. We speculate here that NO may also participate in the pain-inhibiting descending inhibitory system of the brainstem. In this experiment, the injection of formalin in the soles of feet caused ipsilateral spinal cord lumbar dorsal horn neuronal nociceptive c fos expression, combined with intrathecal injection of nitric oxide synthase inhibitor method to observe whether NO is involved in spinal dorsal horn neuron pain Reaction and the suppression of the reaction to the downstream activity. The first part of the experiment shows that injection of formalin on the paw sidefoot can cause nociceptive c fos expression in the lumbar dorsal horn of ipsilateral spinal cord; intrathecal injection of nitric oxide synthase inhibitor L-NNA arginine Inhibit its expression dependently. In the second part of the experiment, the first half of the spinal cord thoracic surgery on one side of the severed operation, and then both feet were injected formalin, at this time shows intact lateral spinal cord c fos expression was significantly less Injury side. This difference can only be explained as intact side preservation issued by the brain stem, downward projection to the spinal lumbar enlargement of the analgesia inhibition of the lateral dorsal c fos expression results; further experiments show that this inhibition can be intrathecal Inject L NNA Cancel. This result indicates that NO not only facilitates the transmission of nociceptive signals at the spinal cord level, but also enhances the effect of a downward inhibitory system of pain.