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首页> 外文期刊>Behavioural Brain Research: An International Journal >Nitric oxide donor molsidomine promotes retrieval of object recognition memory in a model of cognitive deficit induced by 192 IgG-saporin
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Nitric oxide donor molsidomine promotes retrieval of object recognition memory in a model of cognitive deficit induced by 192 IgG-saporin

机译：一氧化氮供体莫里西亚甲酰胺促进在192 IgG-Saporin诱导的认知缺陷模型中的物体识别记忆中的检索

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摘要

Nitric oxide (NO) plays a leading role in learning and memory processes. Previously, we showed its ability to modify the deleterious effect of immunotoxin 192 IgG-saporin (192-IgG-SAP) in the cholinergic system. The aim of this study was to analyze the potential of a NO donor (molsidomine, MOLS) to prevent the recognition memory deficits resulting from the septal cholinergic denervation by 192 IgG-SAP in rats. Quantification of neuronal and endothelial nitric oxide synthase (nNOS and eNOS, respectively) expression was evaluated in striatum, prefrontal cortex, and hippocampus. In addition, a choline acetyltransferase immunohistochemical analysis was performed in medial septum and assessed the effect of MOLS treatment on the spatial working memory of rats through a recognition memory test. Results showed that 192-IgG-SAP reduced the immunoreactivity of cholinergic septal neurons (41%), compared with PBS-receiving control rats (p < 0.05). Treatment with MOLS alone failed to antagonize the septal neuron population loss but prevented the progressive abnormal morphological changes of neurons. Those animals exposed to 192-IgG-SAP immunotoxin exhibited a reduction of cortical nNOS expression against the control group, whereas expression was enhanced in the 192-IgG-SAP + MOLS group. The most relevant finding was the recovering of the discrimination index exhibited by the 192-IgG-SAP + MOLS group. When compared with the rats exposed to the 192-IgG-SAP immunotoxin, they reached values similar to those observed in the PBS group. Our results show that although MOLS failed to block the cholinergic neurons loss induced by 192-IgG-SAP, it avoided the neuronal damage progression.
机译：一氧化氮（NO）在学习和记忆过程中起着主导作用。以前，我们展示了能够改变免疫毒素192 IgG-Saporin（192-IgG-SAP）在胆碱能系统中的有害效果的能力。本研究的目的是分析NO供体（Molsidomine，Mols）的潜力，以防止由192 IgG-SAP中的隔膜胆碱能除去导致的识别记忆缺陷。在纹状体，前额叶皮质和海马中评估了神经元和内皮酰化合酶（分别）表达的神经元和内皮酰化合酶（NNOS和enos）。此外，在内侧隔膜中进行胆碱乙酰转移酶免疫组化分析，并评估摩尔治疗在大鼠空间工作记忆中通过识别记忆试验的影响。结果表明，与PBS接受对照大鼠相比，192-IgG-SAP减少了胆碱能子神经元（41％）的免疫反应性（P <0.05）。单独用摩尔治疗未能拮抗子宫内膜群体损失，但预防神经元的逐步异常形态变化。暴露于192-IgG-SAP免疫毒素的那些动物表现出对对照组的皮质NNO表达的减少，而在192-IgG-SAP +摩尔基团中提高了表达。最相关的发现是回收192-IgG-SAP +摩尔组展出的歧视指数。与暴露于192-IgG-SAP免疫毒素的大鼠相比，它们达到与PBS组中观察到的大鼠类似的值。我们的研究结果表明，尽管摩尔未能阻断192-IgG-SAP诱导的胆碱能神经元损失，但它避免了神经元损伤进展。

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