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工作记忆系统的可塑性:寿命变化和对损伤的反应。

Plasticity in the Working Memory System: Life Span Changes and Response to Injury.

机构信息

1 Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

2 Cognitive Neurology and Aphasia Unit and Cathedra ARPA of Aphasia, Centro de Investigaciones Médico-Sanitarias (CIMES) and Instituto de Investigación Biomédica de Malaga, University of Malaga, Malaga, Spain.

出版信息

Neuroscientist. 2018 Jun;24(3):261-276. doi: 10.1177/1073858417717210. Epub 2017 Jul 8.

DOI:10.1177/1073858417717210
PMID:28691573
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8647815/
Abstract

Working memory acts as a key bridge between perception, long-term memory, and action. The brain regions, connections, and neurotransmitters that underlie working memory undergo dramatic plastic changes during the life span, and in response to injury. Early life reliance on deep gray matter structures fades during adolescence as increasing reliance on prefrontal and parietal cortex accompanies the development of executive aspects of working memory. The rise and fall of working memory capacity and executive functions parallels the development and loss of neurotransmitter function in frontal cortical areas. Of the affected neurotransmitters, dopamine and acetylcholine modulate excitatory-inhibitory circuits that underlie working memory, are important for plasticity in the system, and are affected following preterm birth and adult brain injury. Pharmacological interventions to promote recovery of working memory abilities have had limited success, but hold promise if used in combination with behavioral training and brain stimulation. The intense study of working memory in a range of species, ages and following injuries has led to better understanding of the intrinsic plasticity mechanisms in the working memory system. The challenge now is to guide these mechanisms to better improve or restore working memory function.

摘要

工作记忆充当了感知、长期记忆和行动之间的关键桥梁。在整个生命周期中,工作记忆的大脑区域、连接和神经递质会发生巨大的可塑性变化,并对损伤做出反应。在青少年时期,对深层灰质结构的早期依赖会逐渐减少,而随着执行功能方面工作记忆的发展,对前额叶和顶叶皮层的依赖会增加。工作记忆容量和执行功能的上升和下降与额叶皮质区域神经递质功能的发展和丧失相吻合。在受影响的神经递质中,多巴胺和乙酰胆碱调节着工作记忆的兴奋-抑制回路,对系统的可塑性很重要,并且在早产儿和成年脑损伤后会受到影响。促进工作记忆能力恢复的药物干预收效甚微,但如果与行为训练和脑刺激结合使用,仍有希望取得成功。在一系列物种、年龄和受伤后的工作记忆的深入研究,使人们更好地理解了工作记忆系统中的内在可塑性机制。现在的挑战是引导这些机制,以更好地改善或恢复工作记忆功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e7d/8647815/6bac71df4486/nihms-1757540-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e7d/8647815/ec9e54878ea4/nihms-1757540-f0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e7d/8647815/6bac71df4486/nihms-1757540-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e7d/8647815/ec9e54878ea4/nihms-1757540-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e7d/8647815/10644b96f6ea/nihms-1757540-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e7d/8647815/5eeb916e14a4/nihms-1757540-f0003.jpg
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