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首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Inaugural Article: Parallel memory processing by the CA1 region of the dorsal hippocampus and the basolateral amygdala
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Inaugural Article: Parallel memory processing by the CA1 region of the dorsal hippocampus and the basolateral amygdala

机译：就职文章：背海马CA1区和基底外侧杏仁核的并行记忆处理

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There is abundant literature on the role of the basolateral amygdala (BLA) and the CA1 region of the hippocampus in memory formation of inhibitory avoidance (IA) and other behaviorally arousing tasks. Here, we investigate molecular correlates of IA consolidation in the two structures and their relation to NMDA receptors (NMDArs) and β-adrenergic receptors (β-ADrs). The separate posttraining administration of antagonists of NMDAr and β-ADr to BLA and CA1 is amnesic. IA training is followed by an increase of the phosphorylation of calcium and calmodulin-dependent protein kinase II (CaMKII) and ERK2 in CA1 but only an increase of the phosphorylation of ERK2 in BLA. The changes are blocked by NMDAr antagonists but not β-ADr antagonists in CA1, and they are blocked by β-ADr but not NMDAr antagonists in BLA. In addition, the changes are accompanied by increased phosphorylation of tyrosine hydroxylase in BLA but not in CA1, suggesting that β-AD modulation results from local catecholamine synthesis in the former but not in the latter structure. NMDAr blockers in CA1 do not alter the learning-induced neurochemical changes in BLA, and β-ADr blockade in BLA does not hinder those in CA1. When put together with other data from the literature, the present findings suggest that CA1 and BLA play a role in consolidation, but they operate to an extent in parallel, suggesting that each is probably involved with different aspects of the task studied.
机译：关于基底外侧杏仁核（BLA）和海马CA1区在记忆形成的抑制性回避（IA）和其他行为激发任务中的作用，已有大量文献报道。在这里，我们研究了IA固结在两个结构中的分子相关性，以及它们与NMDA受体（NMDArs）和β-肾上腺素受体（β-ADrs）的关系。 NMDAr和β-ADr拮抗剂分别对BLA和CA1的训练后记忆消除。 IA训练后，CA1中钙和钙调蛋白依赖性蛋白激酶II（CaMKII）和ERK2的磷酸化增加，但BLA中ERK2的磷酸化仅增加。在CA1中，这些变化被NMDAr拮抗剂阻断，但未被β-ADr拮抗剂阻断；而在BLA中，它们被β-ADr阻断但未被NMDAr拮抗剂阻断。此外，这些变化伴随着BLA中而不是CA1中酪氨酸羟化酶的磷酸化增加，这表明前者中局部儿茶酚胺合成引起β-AD调节，而后者则不。 CA1中的NMDAr阻滞剂不会改变学习引起的BLA神经化学变化，而BLA中的β-ADr阻滞不会阻碍CA1中的神经化学变化。当与文献中的其他数据放在一起时，本研究结果表明CA1和BLA在整合中发挥了作用，但它们在一定程度上并行运行，这表明每种可能涉及所研究任务的不同方面。

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