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电针刺激内嗅皮层改善 AD 模型大鼠学习记忆能力及海马突触可塑性

Post-training intra-basolateral amygdala infusions of norepinephrine block sevoflurane-induced impairment of memory consolidation and activity-regulated cytoskeletal protein expression inhibition in rat hippocampus.

机构信息

Department of Anesthesiology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200025, PR China.

出版信息

Neurobiol Learn Mem. 2011 Oct;96(3):492-7. doi: 10.1016/j.nlm.2011.08.002. Epub 2011 Aug 22.

DOI:10.1016/j.nlm.2011.08.002
PMID:21872671
Abstract

Considerable evidence indicates that the noradrenergic system of the basolateral amygdala (BLA) participates in the consolidation of various types of emotionally arousing memories. We previously reported that administration of an anesthetic-dose of sevoflurane immediately after continuous multiple-trail inhibition avoidance (CMIA) training impaired memory consolidation. This experiment investigated whether posttraining noradrenergic activation of the BLA is sufficient to reverse the memory impairing effect of sevoflurane. Adult male Sprague-Dawley rats received bilateral injections of norepinephrine (NE 0.3, 1.0, or 3.0 μg/0.5 μl) or normal saline (NS 0.5 μl) immediately after training in a CMIA paradigm. Subsequently, the rats were exposed to sevoflurane (2% inspired) or air for 2h. Norepinephrine produced a dose-dependent enhancement of memory consolidation on a 24-h retention test. The highest dose of NE tested (3.0 μg/0.5 μl) blocked sevoflurane-induced impairment of memory consolidation and reversed the inhibitory effect of sevoflurane on activity-regulated cytoskeletal protein (Arc) expression in the hippocampus 2h after training. These findings provide evidence that the mechanism mediating the memory-impairing effect of sevoflurane involves a network interaction between the BLA noradrenergic system and modulation of Arc protein expression in the hippocampus.

摘要

大量证据表明,外侧杏仁核(BLA)的去甲肾上腺素能系统参与了各种情绪唤醒记忆的巩固。我们之前的研究表明,连续多次回避(CMIA)训练后立即给予麻醉剂量的七氟醚会损害记忆巩固。本实验研究了 BLA 的去甲肾上腺素能激活是否足以逆转七氟醚对记忆的损害作用。成年雄性 Sprague-Dawley 大鼠在 CMIA 范式中接受双侧去甲肾上腺素(NE 0.3、1.0 或 3.0μg/0.5μl)或生理盐水(NS 0.5μl)注射,随后暴露于七氟醚(2%吸入)或空气中 2 小时。去甲肾上腺素在 24 小时保留测试中产生了剂量依赖性的记忆巩固增强作用。测试的最高剂量 NE(3.0μg/0.5μl)阻断了七氟醚引起的记忆巩固损伤,并逆转了七氟醚对训练后 2 小时海马体中活性调节细胞骨架蛋白(Arc)表达的抑制作用。这些发现为介导七氟醚致记忆损伤作用的机制提供了证据,该机制涉及 BLA 去甲肾上腺素能系统与海马体中 Arc 蛋白表达的调节之间的网络相互作用。

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