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John L. Dart Library
9 a.m. – 7 p.m.
Phone: (843) 722-7550
West Ashley Library
9 a.m. – 7 p.m.
Phone: (843) 766-6635
Folly Beach Library
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Phone: (843) 588-2001
Edgar Allan Poe/Sullivan's Island Library
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Phone: (843) 883-3914
Wando Mount Pleasant Library
9 a.m. – 8 p.m.
Phone: (843) 805-6888
Village Library
9 a.m. – 6 p.m.
Phone: (843) 884-9741
St. Paul's/Hollywood Library
9 a.m. – 8 p.m.
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Otranto Road Library
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Phone: (843) 572-4094
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9 a.m. – 8 p.m.
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McClellanville Library
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Phone: (843) 805-6930
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ERG3 potassium channel‐mediated suppression of neuronal intrinsic excitability and prevention of seizure generation in mice.
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- Author(s): Xiao, Kuo; Sun, Zhiming; Jin, Xueqin; Ma, Weining; Song, Yan; Lai, Shirong; Chen, Qian; Fan, Minghua; Zhang, Jingliang; Yue, Weihua; Huang, Zhuo
- Source:
Journal of Physiology; Oct2018, Vol. 596 Issue 19, p4729-4752, 24p- Subject Terms:
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- Additional Information
- Abstract: Key points: ERG3 channels have a high expression level in the central nervous system. Knockdown of ERG3 channels enhances neuronal intrinsic excitability (caused by decreased fast afterhyperpolarization, shortened delay time to the generation of an action potential and enhanced summation of somatic excitatory postsynaptic potentials) in hippocampal CA1 pyramidal neurons and dentate gyrus granule cells. The expression of ERG3 protein is reduced in human and mouse hippocampal epileptogenic foci. Knockdown of ERG3 channels in hippocampus enhanced seizure susceptibility, while mice treated with the ERG channel activator NS‐1643 were less prone to epileptogenesis. The results provide strong evidence that ERG3 channels have a crucial role in the regulation of neuronal intrinsic excitability in hippocampal CA1 pyramidal neurons and dentate gyrus granule cells and are critically involved in the onset and development of epilepsy. Abstract: The input–output relationship of neuronal networks depends heavily on the intrinsic properties of their neuronal elements. Profound changes in intrinsic properties have been observed in various physiological and pathological processes, such as learning, memory and epilepsy. However, the cellular and molecular mechanisms underlying acquired changes in intrinsic excitability are still not fully understood. Here, we demonstrate that ERG3 channels are critically involved in the regulation of intrinsic excitability in hippocampal CA1 pyramidal neurons and dentate gyrus granule cells. Knock‐down of ERG3 channels significantly increases neuronal intrinsic excitability, which is mainly caused by decreased fast afterhyperpolarization, shortened delay time to the generation of an action potential and enhanced summation of somatic excitatory postsynaptic potentials. Interestingly, the expression level of ERG3 protein is significantly reduced in human and mouse brain tissues with temporal lobe epilepsy. Moreover, ERG3 channel knockdown in hippocampus significantly enhanced seizure susceptibility, while mice treated with the ERG channel activator NS‐1643 were less prone to epileptogenesis. Taken together, our results suggest ERG3 channels play an important role in determining the excitability of hippocampal neurons and dysregulation of these channels may be involved in the generation of epilepsy. ERG3 channels may thus be a novel therapeutic target for the prevention of epilepsy. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Journal of Physiology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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