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首页> 外文期刊>The European Journal of Neuroscience >Adenosine preconditions against ouabain but not against glutamate on CA1-evoked potentials in rat hippocampal slices.
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Adenosine preconditions against ouabain but not against glutamate on CA1-evoked potentials in rat hippocampal slices.

机译：在大鼠海马切片中，针对哇巴因的腺苷前提条件而非针对谷氨酸的前提条件是针对谷氨酸盐。

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Hypoxic and ischaemic brain damage are believed to involve excessive release of glutamate, and recent work shows that glutamate-induced damage in brain slices can be reduced by preconditioning with hypoxia or glutamate itself. Because adenosine is a powerful preconditioning agent, we have investigated whether adenosine could precondition against glutamate in vitro. In rat hippocampal slices, glutamate depolarization reduced the amplitudes of antidromic- and orthodromic-evoked potentials, with only partial recovery. Applying adenosine before these insults failed to increase that recovery. Ouabain also produced depolarization with partial reversibility, but adenosine pretreatment increased the extent of recovery. The preconditioning effect of adenosine on ouabain responses was prevented by blocking receptors for N-methyl-D-aspartate (NMDA), but not receptors for kainate or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and was blocked by inhibiting nitric oxide synthase. Preconditioningwas also abolished by the ATP-dependent potassium channel blockers, glibenclamide (cytoplasmic) or 5-hydroxydecanoate (mitochondrial). We conclude that adenosine does not precondition against glutamate in hippocampal slices, but that it does precondition against ouabain with a pharmacology similar to studies in vivo. Ischaemic neuronal damage is a complex of many factors, and because adenosine can precondition against ischaemic neuronal damage, its failure to protect against glutamate highlights limitations of using glutamate alone as a model for ischaemia. Because damage following ischaemia, trauma or excitotoxicity also involves reduced Na(+),K(+)-ATPase activity, and adenosine can precondition against ouabain, we propose that ouabain-induced damage represents an additional or alternative model for the contribution to cell damage of Na(+),K(+)-ATPase loss, this being more relevant to the mechanisms of preconditioning.
机译：缺氧和缺血性脑损伤被认为与谷氨酸的过度释放有关，最近的研究表明，通过缺氧或谷氨酸本身的预处理可以减少谷氨酸对脑片的损害。由于腺苷是一种强大的预处理剂，因此我们研究了腺苷是否可以在体外对谷氨酸进行预处理。在大鼠海马切片中，谷氨酸去极化降低了抗驱和正驱诱发电位的幅度，仅部分恢复。在这些侮辱之前应用腺苷不能增加这种恢复。瓦巴因也产生了具有部分可逆性的去极化，但是腺苷预处理增加了恢复的程度。通过阻断N-甲基-D-天冬氨酸（NMDA）的受体阻止腺苷对ouabain反应的预处理作用，但不阻止海藻酸盐或α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）的受体，并通过抑制一氧化氮合酶被阻断。 ATP依赖性钾通道阻滞剂，格列本脲（胞质）或5-羟基癸酸酯（线粒体）也取消了预处理。我们得出的结论是，腺苷不是针对海马片中的谷氨酸的先决条件，但它是针对哇巴因的先决条件，其药理作用类似于体内研究。缺血性神经元损害是许多因素的复合物，并且由于腺苷可以预防缺血性神经元损害，因此其无法防御谷氨酸盐突出了仅使用谷氨酸盐作为局部缺血模型的局限性。由于局部缺血，创伤或兴奋性中毒后的损伤也涉及Na（+），K（+）-ATPase活性降低，并且腺苷可以预防哇巴因，因此我们建议哇巴因诱导的损伤代表了对细胞损伤的额外或替代模型Na（+），K（+）-ATPase的损失，这与预处理的机制更相关。

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