Methylglyoxal (MGO) is a highly reactive dicarbonyl molecule that promotes the formation of advanced glycation end products (AGEs), which are believed to play a key role in a number of pathologies, such as diabetes, Alzheimer's disease, and inflammation. Here, Swiss mice were treated with MGO by intraperitoneal injection to investigate its effects on motor activity, mood, and cognition. Acute MGO treatment heavily decreased locomotor activity in the open field test at higher doses (80-200 mg/kg), an effect not observed at lower doses (10-50 mg/kg). Several alterations were observed 4 h after a single MGO injection (10-50 mg/kg): (a) plasma MGO levels were increased, (b) memory was impaired (object location task), (c) anxiolytic behavior was observed in the open field and marble burying test, and (d) depressive-like behavior was evidenced as evaluated by the tail suspension test. Biochemical alterations in the glutathione and glyoxalase systems were not observed 4 h after MGO treatment. Mice were also treated daily with MGO at 0, 10, 25 and 50 mg/kg for 11 days. From the 5th to the 11th day, several behavioral end points were evaluated, resulting in: (a) absence of motor impairment as evaluated in the open field, horizontal bars and pole test, (b) depressive-like behavior observed in the tail suspension test, and (c) cognitive impairments detected on working, short- and long-term memory when mice were tested in the Y-maze spontaneous alternation, object location and recognition tests, and step-down inhibitory avoidance task. An interesting finding was a marked decrease in dopamine levels in the prefrontal cortex of mice treated with 50 mg/kg MGO for 11 days, along with a ~ 25% decrease in the Glo1 content. The MGO-induced dopamine depletion in the prefrontal cortex may be related to the observed memory deficits and depressive-like behavior, an interesting topic to be further studied as a potentially novel route for MGO toxicity.

中文翻译：

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重复的甲基乙二醛治疗会耗尽前额叶皮层中的多巴胺，并导致小鼠记忆力减退和抑郁样行为。

甲基乙二醛（MGO）是一种高反应性的二羰基分子，可促进高级糖基化终产物（AGEs）的形成，而后者被认为在许多病理学中起着关键作用，例如糖尿病，阿尔茨海默氏病和炎症。在这里，瑞士小鼠通过腹膜内注射MGO进行治疗，以研究其对运动活动，情绪和认知的影响。急性MGO治疗在大剂量（80-200 mg / kg）的大田野试验中严重降低了运动活性，而在小剂量（10-50 mg / kg）下未观察到这种作用。单次MGO注射（10-50 mg / kg）后4小时，观察到一些变化：（a）血浆MGO水平升高，（b）记忆力受损（对象定位任务），（c）在小鼠体内观察到抗焦虑行为。露天和大理石掩埋测试，（d）通过尾部悬架测试评估了抑郁样行为。MGO处理后4小时未观察到谷胱甘肽和乙二醛酶系统的生化变化。还每天用0、10、25和50 mg / kg的MGO对小鼠进行治疗11天。从第5天到第11天，对几个行为终点进行了评估，结果是：（a）在开阔场地，水平杠和杆测试中没有发现运动障碍，（b）在尾部悬架中观察到了类似抑郁的行为测试，以及（c）在Y迷宫自发交替，对象定位和识别测试以及降低抑制回避任务中对小鼠进行测试时，在工作，短期和长期记忆上检测到认知障碍。一个有趣的发现是用50 mg / kg MGO治疗11天的小鼠前额叶皮层中的多巴胺水平显着降低，并且Glo1含量降低了约25％。MGO诱导的前额叶皮层中的多巴胺消耗可能与观察到的记忆缺陷和抑郁样行为有关，这是一个有趣的话题，有待进一步研究，作为MGO毒性的潜在新途径。