大鼠海马切片中*NO 和 O2 的动态相互作用谱。
Dynamic and interacting profiles of *NO and O2 in rat hippocampal slices.
机构信息
Center for Neurosciences and Cell Biology, University of Coimbra, 3000 Coimbra, Portugal.
出版信息
Free Radic Biol Med. 2010 Apr 15;48(8):1044-50. doi: 10.1016/j.freeradbiomed.2010.01.024. Epub 2010 Jan 25.
Abstract
Nitric oxide (*NO) is a ubiquitous signaling molecule that participates in the neuromolecular phenomena associated with memory formation. In the hippocampus, neuronal *NO production is coupled to the activation of the NMDA-type of glutamate receptor. Although *NO-mediated signaling has been associated with soluble guanylate cyclase activation, cytochrome oxidase is also a target for this gaseous free radical, for which *NO competes with O(2). Here we show, for the first time in a model preserving tissue cytoarchitecture (rat hippocampal slices) and at a physiological O(2) concentration, that endogenous NMDA-evoked *NO production inhibits tissue O(2) consumption for submicromolar concentrations. The simultaneous real-time recordings reveal a direct correlation between the profiles of *NO and O(2) in the CA1 subregion of the hippocampal slice. These results, obtained in a system close to in vivo models, strongly support the current paradigm for O(2) and *NO interplay in the regulation of cellular respiration.
摘要
一氧化氮（NO）是一种普遍存在的信号分子，参与与记忆形成相关的神经分子现象。在海马体中，神经元NO 的产生与 NMDA 型谷氨酸受体的激活相关联。尽管NO 介导的信号与可溶性鸟苷酸环化酶的激活有关，但细胞色素氧化酶也是这种气态自由基的靶标，NO 与 O(2)竞争。在这里，我们首次在保持组织细胞结构（大鼠海马切片）和生理 O(2)浓度的模型中表明，内源性 NMDA 诱发的NO 产生抑制了组织 O(2)的消耗，其浓度低至亚微米。同时进行的实时记录揭示了海马切片 CA1 区NO 和 O(2)的特征之间存在直接相关性。这些在接近体内模型的系统中获得的结果，强烈支持了目前关于 O(2)和*NO 相互作用在细胞呼吸调节中的范式。
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