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K7通道在神经可塑性和行为中的作用。

The Role of K7 Channels in Neural Plasticity and Behavior.

作者信息

Baculis Brian C, Zhang Jiaren, Chung Hee Jung

机构信息

Neuroscience Program, University of Illinois at Urbana-Champaign, Urbana, IL, United States.

Department of Molecular Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana, IL, United States.

出版信息

Front Physiol. 2020 Sep 18;11:568667. doi: 10.3389/fphys.2020.568667. eCollection 2020.

DOI:10.3389/fphys.2020.568667
PMID:33071824
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7530275/
Abstract

Activity-dependent persistent changes in neuronal intrinsic excitability and synaptic strength are widely thought to underlie learning and memory. Voltage-gated KCNQ/K7 potassium channels have been of great interest as the potential targets for memory disorders due to the beneficial effects of their antagonists in cognition. Importantly, dominant mutations in their neuronal subunits /K7.2 and /K7.3 are associated with epilepsy and neurodevelopmental disorder characterized by developmental delay and intellectual disability. The role of K7 channels in neuronal excitability and epilepsy has been extensively studied. However, their functional significance in neural plasticity, learning, and memory remains largely unknown. Here, we review recent studies that support the emerging roles of K7 channels in intrinsic and synaptic plasticity, and their contributions to cognition and behavior.

摘要

神经元内在兴奋性和突触强度的活动依赖性持续变化被广泛认为是学习和记忆的基础。电压门控KCNQ/K7钾通道因其拮抗剂在认知方面的有益作用而成为记忆障碍的潜在靶点,备受关注。重要的是,其神经元亚基K7.2和K7.3中的显性突变与癫痫以及以发育迟缓、智力残疾为特征的神经发育障碍有关。K7通道在神经元兴奋性和癫痫中的作用已得到广泛研究。然而,它们在神经可塑性、学习和记忆中的功能意义仍 largely unknown。在此,我们综述了最近的研究,这些研究支持了K7通道在内在和突触可塑性中的新作用,以及它们对认知和行为的贡献。 (注:“largely unknown”直译为“很大程度上未知”,这里意译为“仍不清楚”更符合语境)

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b4f/7530275/7fd95cd36b05/fphys-11-568667-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b4f/7530275/7fd95cd36b05/fphys-11-568667-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b4f/7530275/7fd95cd36b05/fphys-11-568667-g001.jpg

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J Neurosci. 2020 May 6;40(19):3694-3706. doi: 10.1523/JNEUROSCI.1914-19.2020. Epub 2020 Apr 10.
3
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Int J Mol Sci. 2025 Feb 11;26(4):1504. doi: 10.3390/ijms26041504.
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