Investigation of the descending noradrenergic Inhibitory pathway using nitrous oxide as a probe

最近的研究表明，氧化亚氮可以激活脑干的去甲肾上腺素能神经元和脊髓的gaba能神经元。然而，介导这些事件的确切神经通路仍有待确定。在成年雄性Fischer大鼠中，脑干去甲肾上腺素能核被脑室内应用抗dssh皂苷选择性损伤。然后将大鼠暴露于氧化亚氮中，检测脊髓gaba能神经元的c-Fos免疫染色。与未破坏去肾上腺素能核的对照组相比，抗dssh皂苷处理大鼠Fos免疫反应性降低。这一结果表明，脑干的去甲肾上腺素能核是氧化亚氮激活脊髓gaba能神经元所必需的。在接下来的研究中，成年雄性Fischer大鼠被给予α-螺旋CRH（促肾上腺皮质激素释放因子受体拮抗剂），DAMGO（阿片受体激动剂）和纳洛酮（阿片受体拮抗剂）脑室内。然后暴露于氧化亚氮，检测脑干去肾上腺素能核（蓝斑核）的c-Fos免疫反应性。大鼠α-螺旋CRH和纳洛酮注射后c-Fos免疫反应性降低，提示促肾上腺皮质激素释放因子和阿片样物质都参与了脑干去甲肾上腺素能神经元的激活。

Recent studies have revealed that nitrous oxide activates noradrenergic neurons in the brain stem and GABAergic neurons in the spinal cord. However, the precise neuronal pathways that mediate these events remain to be determined.In adult male Fischer rats, noradrenergic nuclei of the brain stem were selectively lesioned by intracerebroventricular application of anti-DssH-saporin. After that rats were exposed to nitrous oxide, and c-Fos immunostaining of GABAergic neurons was examined in the spinal cord. Fos immunoreactivity was diminished in the anti-DssH-saporin treated rats than control rats which were not destroyed noradrenergic nuclei. This result shows that noradrenergic nuclei of the brain stem are essential for nitrous oxide to activate GABAergic neurons in the spinal cord.In the following study, adult male Fischer rats were administered α-helical CRH (a corticotropin releasing factor receptor antagonist), DAMGO (an opioid receptor agonist), and naloxne (an opioid receptor antagonist) intracerebroventricularly. Then they were exposed to nitrous oxide, and c-Fos immunoreactivity of brain stem noradrenergic nucleus (locus coeruleus) was examined. Diminishing of c-Fos immunoreactivity inα-helical CRH and naloxone administered rats suggests that both corticotropin releasing factor and opioid are involved in the activation of noradrenergic neurons in the brain stem.