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首页> 外文期刊>The European Journal of Neuroscience >Exogenous agmatine has neuroprotective effects against restraint-induced structural changes in the rat brain.
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Exogenous agmatine has neuroprotective effects against restraint-induced structural changes in the rat brain.

机译：外源胍丁胺具有神经保护作用，可抑制大鼠大脑中由约束诱导的结构变化。

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摘要

Agmatine is an endogenous amine derived from decarboxylation of arginine catalysed by arginine decarboxylase. Agmatine is considered a novel neuromodulator and possesses neuroprotective properties in the central nervous system. The present study examined whether agmatine has neuroprotective effects against repeated restraint stress-induced morphological changes in rat medial prefrontal cortex and hippocampus. Sprague-Dawley rats were subjected to 6 h of restraint stress daily for 21 days. Immunohistochemical staining with beta-tubulin III showed that repeated restraint stress caused marked morphological alterations in the medial prefrontal cortex and hippocampus. Stress-induced alterations were prevented by simultaneous treatment with agmatine (50 mg/kg/day, i.p.). Interestingly, endogenous agmatine levels, as measured by high-performance liquid chromatography, in the prefrontal cortex and hippocampus as well as in the striatum and hypothalamus of repeated restraint rats were significantly reduced as compared with the controls. Reduced endogenous agmatine levels in repeated restraint animals were accompanied by a significant increase of arginine decarboxylase protein levels in the same regions. Moreover, administration of exogenous agmatine to restrained rats abolished increases of arginine decarboxylase protein levels. Taken together, these results demonstrate that exogenously administered agmatine has neuroprotective effects against repeated restraint-induced structural changes in the medial prefrontal cortex and hippocampus. These findings indicate that stress-induced reductions in endogenous agmatine levels in the rat brain may play a permissive role in neuronal pathology induced by repeated restraint stress.
机译：胍丁胺是由精氨酸脱羧酶催化的精氨酸脱羧衍生的内源性胺。胍丁胺被认为是一种新型的神经调节剂，在中枢神经系统中具有神经保护特性。本研究检查了胍丁胺是否对大鼠内侧前额叶皮层和海马体中的重复约束应激诱导的形态学改变具有神经保护作用。每天对Sprague-Dawley大鼠施加6小时的束缚压力，持续21天。用β-微管蛋白III进行的免疫组织化学染色显示，反复的约束压力导致内侧前额叶皮层和海马体的形态发生明显改变。通过同时用胍丁胺（50 mg / kg /天，腹膜内注射）治疗，可以防止压力引起的变化。有趣的是，与对照相比，用高效液相色谱法测定的反复约束大鼠的前额叶皮层和海马以及纹状体和下丘脑中的内源胍丁胺水平显着降低。在重复约束动物中内源性胍丁胺水平的降低伴随着相同区域精氨酸脱羧酶蛋白水平的显着增加。此外，向受约束的大鼠施用外源胍丁胺消除了精氨酸脱羧酶蛋白水平的增加。综上所述，这些结果表明，外源性胍丁胺具有神经保护作用，可防止内前额叶皮层和海马体反复受到约束诱导的结构变化。这些发现表明，应激诱导的大鼠大脑内源性胍丁胺水平的降低可能在反复约束应激诱导的神经元病理学中发挥了重要作用。

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