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Pharmacological findings contribute to the understanding of the main physiological mechanisms of memory retrieval.

机译:药理学发现有助于理解记忆恢复的主要生理机制。

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Recent pharmacological findings have shown that retrieval of one-trial avoidance learning requires glutamate receptors, cAMP-dependent protein kinase and mitogen-activated protein kinases in the hippocampus, entorhinal, posterior parietal and anterior cingulate cortex. It requires AMPA but not other type of glutamate receptors or the protein kinases in the amygdala. Retrieval is modulated by dopamine D1, beta-noradrenergic, serotonin 1A and cholinergic receptors in the four cortical structures mentioned, and by beta-noradrenergic receptors in the basolateral amygdala. Further, retrieval is also modulated by peripheral ACTH, glucocorticoids, vasopressin, beta-endorphin and catecholamines; these hormones probably act through beta-noradrenergic receptor systems in the basolateral amygdala. Exposure to novelty or the systemic administration of antidepressant drugs prior to retention tests enhances retrieval, even for very remote memories. The effect of novelty is mediated by molecular mechanisms similar tothose of retrieval itself.
机译:最近的药理学发现表明,一次回避学习的检索需要海马,内嗅,顶叶后壁和前扣带回皮层中的谷氨酸受体,依赖cAMP的蛋白激酶和促分裂原激活的蛋白激酶。它需要AMPA,但不需要其他类型的谷氨酸受体或杏仁核中的蛋白激酶。所述的检索是由提到的四个皮质结构中的多巴胺D1,β-去甲肾上腺素能,5-羟色胺1A和胆碱能受体以及基底外侧杏仁核中的β-去甲肾上腺素能受体调节的。此外,还通过外周ACTH,糖皮质激素,血管加压素,β-内啡肽和儿茶酚胺调节回收。这些激素可能通过基底外侧杏仁核中的β-去甲肾上腺素能受体系统起作用。在保留测试之前接触新颖性药物或抗抑郁药的全身给药可提高检索效率,即使对于非常遥远的记忆也是如此。新颖性的影响是由类似于检索本身的分子机制介导的。

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