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Methylphenidate induces state-dependency of social recognition learning: Central components

机译：甲基苯胺诱导社会认可学习的国家依赖性：中央组件

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摘要

Methylphenidate (MPH) is a widely prescribed drug for the treatment of attention-deficit hyperactivity disorder. Findings in the literature suggest that the effects of MPH on memory may result from increased extracellular levels of norepinephrine (NE) and dopamine (DA). Here, we report that the systemic administration of MPH before the acquisition phase in a social discrimination task impaired the retrieval of the social recognition memory (SRM), but made it state-dependent: another administration of MPH before the retention test recovered the SRM. We observed that the induction of state dependency by MPH relies on the ventromedial prefrontal cortex (vmPFC), but not on the CA1 region of the hippocampus (CA1). Also, the inhibitors of NE and DA, nisoxetine and GBR12909, respectively, restored the SRM when infused into the vmPFC. Only the GBR12909 was able to restore the SRM in the CA1, whereas nisoxetine could not restore and even caused an impairment on memory retrieval when infused alone before the retention test. The data suggest that the state-dependence of SRM induced by MPH depends on an influence of both catecholamines on the vmPFC, while NE inhibits the retrieval of SRM on the hippocampus.
机译：甲基酚（MPH）是一种广泛规定的药物，用于治疗注意力缺陷多动障碍。文献中的发现表明，MPH对内存的影响可能是由于脑细胞碱（NO）和多巴胺（DA）的增加。在这里，我们报告说，在社会歧视任务中获取阶段之前的MPH全身管理损害了社会识别记忆（SRM）的检索，而是使其依赖于依赖性：在保留试验中恢复SRM之前的另一个施用MPH。我们观察到，MPH的状态依赖性诱导依赖于口腔前额叶皮质（VMPFC），但不依赖于海马的CA1区域（CA1）。此外，当注入VMPFC时，分别抑制Ne和Da，Nisoxetine和GBR12909的抑制剂恢复了SRM。只有GBR12909能够在CA1中恢复SRM，而Nisoxetine无法恢复，甚至在保留测试之前单独注入时记忆检索造成的损伤。该数据表明，MPH诱导的SRM的状态依赖性取决于儿茶酚胺对VMPFC的影响，而NE抑制海马对SRM的检索。

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