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药理学研究结果有助于理解记忆提取的主要生理机制。

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

作者信息

Barros Daniela M, Izquierdo Luciana A, Medina Jorge H, Izquierdo Ivan

机构信息

Centro de Memória, Departamento de Bioquímica, Instituto de Ciencias Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Ramiro Barcellos, 2600-anexo, 90035-003 Porto Alegre, RS, Brazil.

出版信息

Curr Drug Targets CNS Neurol Disord. 2003 Apr;2(2):81-94. doi: 10.2174/1568007033482931.

DOI:10.2174/1568007033482931
PMID:12769801
Abstract

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 to those of retrieval itself.

摘要

最近的药理学研究结果表明,单次回避学习的提取需要海马体、内嗅皮层、顶叶后部和前扣带回皮层中的谷氨酸受体、环磷酸腺苷依赖性蛋白激酶和丝裂原活化蛋白激酶。它需要α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)受体,但不需要杏仁核中的其他类型谷氨酸受体或蛋白激酶。在上述四个皮层结构中,提取受多巴胺D1、β-去甲肾上腺素能、5-羟色胺1A和胆碱能受体调节,在基底外侧杏仁核中则受β-去甲肾上腺素能受体调节。此外,提取还受外周促肾上腺皮质激素、糖皮质激素、血管加压素、β-内啡肽和儿茶酚胺调节;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发挥作用。在记忆保持测试前接触新事物或全身性给予抗抑郁药物可增强提取,即使对于非常久远的记忆也是如此。新事物的作用是由与提取本身相似的分子机制介导的。

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引用本文的文献

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Increased hippocampal CREB phosphorylation in dopamine D3 receptor knockout mice following passive avoidance conditioning.在被动回避训练后,多巴胺 D3 受体敲除小鼠海马体 CREB 磷酸化增加。
Neurochem Res. 2013 Dec;38(12):2516-23. doi: 10.1007/s11064-013-1164-3. Epub 2013 Oct 8.
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Hippocampal extracellular signal-regulated kinase signaling has a role in passive avoidance memory retrieval induced by GABAA Receptor modulation in mice.
海马细胞外信号调节激酶信号在 GABAA 受体调制诱导的小鼠被动回避记忆检索中起作用。
Neuropsychopharmacology. 2012 Apr;37(5):1234-44. doi: 10.1038/npp.2011.311. Epub 2011 Dec 14.
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Involvement of the beta-endorphin neurons of the hypothalamic arcuate nucleus in ethanol-induced place preference conditioning in mice.下丘脑弓状核β-内啡肽神经元在小鼠乙醇诱导的位置偏爱形成中的作用。
Alcohol Clin Exp Res. 2011 Nov;35(11):2019-29. doi: 10.1111/j.1530-0277.2011.01553.x. Epub 2011 Oct 20.
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Activation of extracellular signal-regulated kinase in the anterior cingulate cortex contributes to the induction and expression of affective pain.前扣带回皮质中细胞外信号调节激酶的激活有助于情感性疼痛的诱导和表达。
J Neurosci. 2009 Mar 11;29(10):3307-21. doi: 10.1523/JNEUROSCI.4300-08.2009.
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J Neural Transm (Vienna). 2007 Mar;114(3):379-85. doi: 10.1007/s00702-006-0585-4. Epub 2006 Oct 27.
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