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Nitric oxide modulates microglial activation

机译：一氧化氮调节小胶质细胞活化

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Background:Nitric oxide (NO) has important physiological regulatory roles, i.e, vasodilation, neurotransmitter release, etc. Little is known about the processes in neural tissues, which stabilize microglia. This study attempts to answer this question by demonstrating a role for basal NO in maintaining microglia juxtaposed to neurons.Material/Methods: Mytilus edulis (a marine bivalve), were used to examine microglia egress from excised pedal ganglia microscopically. Nitric oxide is measured in excised pedal ganglia amperometrically in real-time.Results: Pedal ganglia exhibit basal NO release (1 nM range). Inhibition of basal NO release by L-NAME results in greater numbers of microglia in the incubation medium. This process appears to involve two phases of egress. The first involves a slow egress of microglia, whereas the second, occurring 18 hours later, involves a more rapid release of these cells. Low levels of the NO donor SNAP (1 nM) does not interrupt microglial egress, whereas in the presence of L-NAME it does. Exposing the ganglia to high NO levels for a short period of time inhibits their egress.Conclusions: Spontaneous ganglionic NO release maintains/stabilizes microglia juxtaposed to neurons. Excised ganglia at the various observation periods reveals a transition of constitutive nitric oxide synthase (NOS) to inducible NOS derived NO. It also appears that the microglia in some unknown manner become insensitive to iNOS derived NO since they exhibit enhanced migration during this last phase of the ganglionic NO response. Taken together, NO is involved with regulating microglial activation.
机译：背景：一氧化氮（NO）具有重要的生理调节作用，即血管舒张，神经递质释放等。对于稳定小胶质细胞的神经组织过程知之甚少。这项研究试图通过证明基底NO在维持小胶质细胞与神经元并置中的作用来回答这个问题。材料/方法：食用Mytilus edulis（一种海洋双壳类动物），用于从显微镜下检查切除的踏板神经节的小胶质细胞出。实时测量脚踏板神经节中一氧化氮的含量。结果：踏板神经节表现出基本的NO释放（1 nM范围）。 L-NAME对基础NO释放的抑制导致孵育培养基中的小胶质细胞数量增加。这个过程似乎涉及到出口的两个阶段。第一次涉及小胶质细胞的缓慢排出，而第二次发生在18小时后，涉及这些细胞的更快释放。少量的NO供体SNAP（1 nM）不会干扰小胶质细胞的流出，而在存在L-NAME的情况下会。在短时间内将神经节暴露于高水平的NO会抑制其流出。结论：自发的神经节NO释放可维持/稳定与神经元并列的小胶质细胞。在各个观察期切除的神经节揭示了组成型一氧化氮合酶（NOS）向诱导型NOS衍生的NO的转变。还似乎是，小胶质细胞对iNOS衍生的NO变得不敏感，因为它们在神经节NO响应的最后阶段显示出增强的迁移。两者合计，NO与调节小胶质细胞活化有关。

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