背景 右美托咪定（dexmedetomidine， Dex）是一种新型高效、高选择性的 α2 肾上腺素能受体激动药，具有镇静、镇痛、抗焦虑等作用。大量研究及实验证据表明，Dex具有神经保护的作用。 目的 了解Dex调节长时程突触可塑性的机制，以发挥其在中枢系统性疾病，如术后认知功能障碍（postoperative cognitive dysfunction， POCD）中的神经保护作用。 内容 长时程突触可塑性是学习记忆的分子细胞学机制，而其重要表现形式—长时程增强（long-term potentiation， LTP）又被认为是学习记忆的神经基础。Dex通过增强LTP调节长时程突触可塑性。 趋向 近年来，Dex的神经保护作用备受关注，探索其调节长时程突触可塑性的机制，为其在临床的应用提供新思路。
Background Dexmedetomidine（Dex） is a new effective and highly elective α2 adrenoreceptor agonist， which exhibits the effects of sedation， analgesia， antianxiety. It has showed that Dex has neuroprotective effects. Objective To better understand the neuroprotective effects on the disease of the central nervous system such as postoperative cognitive dysfunction （POCD）. Content Long-term synaptic plasticity is a molecular cytological mechanism of learning and memory. Long-term potentiation （LTP）， as an important manifestation of the long-term synaptic plasticity， is considered as the neural basis of learning and memory. Dex regulate long-term synaptic plasticity via enhancing LTP. Trend Recently， the neuroprotective effect of Dex has received much attention. It's one of the targets of the basic research to study the mechanism of Dex regulating long-term synaptic plasticity and provide new ideas for its clinical application.
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