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首页> 外文期刊>Behavioural Brain Research: An International Journal >Kinetic deterioration of short memory in rat with acute hepatic encephalopathy: Involvement of astroglial and neuronal dysfunctions
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Kinetic deterioration of short memory in rat with acute hepatic encephalopathy: Involvement of astroglial and neuronal dysfunctions

机译：急性肝脑病大鼠短记忆的动力学恶化：颅痛和神经元功能障碍的参与

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Hepatic encephalopathy (HE) is a complex neuropsychiatric syndrome resulting from acute or chronic hepatic impairments. The clinical features of HE include attention as well as a mild cognitive deficits associated with impaired attentional and executive networks in patients as well as in animal models of HE. The underlining pathomechanism of memory impairment in HE patients is still not fully understood; however, it may involve a possible gliopathy as well as neuropathy. The aim of the present investigation is to assess progression of short working memory deterioration in acute HE and to delineate the glial and the neuronal alteration which may underlie such cognitive impairment. The study was carried out in male Sprague-Dawley rats with acute liver failure induced by thioacetamide (TAA). The study was performed on different stages of acute HE; 12 h, 24 h and 36 h following administration of TAA. The liver functions were assessed via different biochemical markers (ALT, AST, bilirubin, urea and creatinine) and an histopathological examination of the liver tissue. While for the behavioral study, we used T-Maze test to assess short working memory using the percentage of alternation behavior, together with an immunohistochemical analysis of the Glial Fibrillary Acidic Protein (GFAP) as the key marker of astrocytes in the hippocampus, as well as serotonin (5-HT) for 5-HTergic neurons within the dorsal Raphe nucleus (DRN). Our data revealed a progressive loss of liver tissue integrity with inflammation and hepatocytes degeneration which was associated to obvious loss of the liver function. In parallel, we observed a gradual alteration of the alternation behavior, as a sign of altered short working memory in the acute HE rats. At the central level, the immunohistochemical study showed a time dependent region-specific changes of GFAP-immunoreactive astrocytes within the hippocampus. While within the DRN, serotonin levels declined progressively in a time-dependant manner. Our data revealed for the first time, a gradual loss of short memory function in acute HE, resulting from liver dysfunction. Such cognitive deterioration may involve a possible gliopathy as well as a 5-HTergic dysfunction which could be considered as a new key element for understanding the basis of memory and attention loss in HE patients.
机译：肝脏脑病（他）是一种复杂的神经精神综合征，由急性或慢性肝损伤引起。他的临床特征包括注意力以及与患者的预造成网络和行政网络有损的轻度认知缺陷以及他的动物模型。患者内存障碍的强调土地机制仍然没有完全理解;然而，它可能涉及可能的神经病变以及神经病变。目前调查的目的是评估急性HE的短期工作记忆恶化的进展，并描绘胶质和神经元改变，这可能使这种认知障碍具有以下。该研究在雄性Sprague-Dawley大鼠进行，硫代乙酰胺（TAA）诱导的急性肝功能失败。该研究是对急性急性阶段进行的;在Taa管理后12小时，24小时和36小时。通过不同的生化标志物（ALT，AST，BiLirubin，尿素和肌酐）和肝组织的组织病理学检查评估肝功能。虽然对于行为研究，我们使用T-Maze试验使用交替行为的百分比来评估短的工作记忆，以及胶质纤维酸性蛋白（GFAP）的免疫组化分析，作为海马的星形胶质细胞的关键标志物，也是如此作为血清核（5-HT）的血清素（5-HT），背甲核（DRN）内的5- htergic神经元。我们的数据揭示了肝组织完整性的逐渐丧失，炎症和肝细胞变性与肝功能明显丧失相关。与此同时，我们观察到交替行为的逐步改变，作为急性肝鼠中的短工作记忆的迹象。在中央层面，免疫组织化学研究显示了海马内的GFAP-免疫反应性星形胶质细胞的时间依赖性区域特异性变化。在DRN内，血清素水平以时间依赖的方式逐渐下降。我们的数据首次揭示，急性肝功能障碍引起的急性内存功能逐渐丧失。这种认知劣化可能涉及可能的神经病症以及5- htergic功能障碍，其可以被认为是了解他患者中记忆和注意力损失的新关键因素。

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