英语翻译Background:Chronic methamphetamine (meth) abuse in humans can lead to various cognitive deficits,including memory loss.We previously showed that chronic meth self-administration impairs memoryfor objects relative to their location and sur

英语翻译Background:Chronic methamphetamine (meth) abuse in humans can lead to various cognitive deficits,including memory loss.We previously showed that chronic meth self-administration impairs memoryfor objects relative to their location and sur
英语翻译
Background:Chronic methamphetamine (meth) abuse in humans can lead to various cognitive deficits,including memory loss.We previously showed that chronic meth self-administration impairs memoryfor objects relative to their location and surrounding objects.Here,we demonstrate that the cognitiveenhancer,modafinil,reversed this cognitive impairment independent of glutamate N-methyl-d-aspartate(GluN) receptor expressionMethods:Male,Long-Evans rats underwent a noncontingent (Experiment 1) or contingent (Experiment2) meth regimen.After one week of abstinence,rats were tested for object-in-place recognition memory.Half the rats received either vehicle or modafinil (100 mg) immediately after object familiarization.Rats (Experiment 2) were sacrificed immediately after the test and brain areas that comprise the keycircuitry for object in place performance were manually dissected.Subsequently,glutamate receptorexpression was measured from a crude membrane fraction using Western blot procedures.Results:Saline-treated rats spent more time interacting with the objects in changed locations,while meth-treated rats distributed their time equally among all objects.Meth-treated rats that received modafinilshowed a reversal in the deficit,whereby they spent more time exploring the objects in the new locations.GluN2B receptor subtype was decreased in the perirhinal cortex,yet remained unaffected in the prefrontalcortex and hippocampus of meth rats.
This meth-induced down regulation occurred whether or not methexperienced rats received vehicle or modafinil.Conclusions:These data support the use of modafinil for memory impairment in meth addiction.Furtherstudies are needed to elucidate the neural mechanisms of modafinil reversal of cognitive impairments.还有补充两句 在此先谢过

英语翻译Background:Chronic methamphetamine (meth) abuse in humans can lead to various cognitive deficits,including memory loss.We previously showed that chronic meth self-administration impairs memoryfor objects relative to their location and sur
背景：人体长期滥用甲基苯丙胺会导致多种认知性缺损,包括记忆力丧失.我们之前已经证明长期甲基自身给药对于记忆的损伤与其区域和周围物质相关.这里,我们演示一下认知增强剂、莫达芬尼等不需依赖谷氨酸NMDA受体表达方法,来修复认知缺损：通过 雄性Long-Evans 大鼠（实验用老鼠）接受必然（实验一）或者偶然（实验二）的甲基方案.停用一周以后,测试老鼠 对适当对象的再认记忆.半数的老鼠在对象熟悉化之后立刻注射相关媒介或者莫达芬尼(100 毫克).测试之后,老鼠们（实验二）立刻死亡,而且包含表现区域对象的关键回路被人工分开.而后,谷氨酸受体表达通过蛋白质印迹法从部分细胞膜内测量.结果：经过盐水处理的老鼠在不同的区域与对象互动需要花费更多的时间,而甲基处理的老鼠则能对对象平等分配时间.注射莫达芬尼的甲基处理的老鼠出现了缺损的修复.因此他们花更多时间探索新区域对象.GluN2B 亚型受体在边缘皮层有所下降,但并不影响甲基鼠前额皮质和海马区.
无论接受了甲基的老鼠是否注射媒介或者莫达芬尼,这种甲基诱发的下调都有可能发生.结论：这些数据可以为使用莫达芬尼修复因甲基成瘾而造成的记忆受损提供依据.详细阐明莫达芬尼对神经机制中认知损伤的可逆性需要进一步的学习.
供参考,我不是学医的,一些医学术语可能翻译的不太准确.

背景：人体长期滥用脱氧麻黄碱会导致各种认知障碍，包括失忆症。我们之前展示了脱氧麻黄碱自我给药损害了目标对象及其周围对象的记忆。这里，我们向您展示提高认知的药物-莫达非尼来对抗这种认知损害，免受谷氨酸n -甲基- d -天门冬氨酸(GluN)受体表达的支配
方法：用雄性Long-Evans 大鼠进行单独（试验1）或批量（试验2）甲基苯丙胺培育。在禁食一周之后，对大鼠进行物品放置认知记忆测试。...

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背景：人体长期滥用脱氧麻黄碱会导致各种认知障碍，包括失忆症。我们之前展示了脱氧麻黄碱自我给药损害了目标对象及其周围对象的记忆。这里，我们向您展示提高认知的药物-莫达非尼来对抗这种认知损害，免受谷氨酸n -甲基- d -天门冬氨酸(GluN)受体表达的支配
方法：用雄性Long-Evans 大鼠进行单独（试验1）或批量（试验2）甲基苯丙胺培育。在禁食一周之后，对大鼠进行物品放置认知记忆测试。 有一半的接受了媒介物或莫达非尼（100毫克）的大鼠立即表现出对物品熟知。 试验2中的大鼠在测试后，支持物品放置认知的关键线路的大脑组成部分被手动解剖了。随后，实验人员用免疫印迹流程通过原油膜对谷氨酸受体表达进行了测量。

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This meth-induced down regulation occurred whether or not methexperienced rats received vehicle or