Enhancement of asynchronous release from fast-spiking interneuron in human and rat epileptic neocortex.

Down-regulation of GABAergic inhibition may result in the generation of epileptiform activities. Besides spike-triggered synchronous GABA release, changes in asynchronous release (AR) following high-frequency discharges may further regulate epileptiform activities. In brain slices obtained from surg...

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Autores principales:	Man Jiang, Jie Zhu, Yaping Liu, Mingpo Yang, Cuiping Tian, Shan Jiang, Yonghong Wang, Hui Guo, Kaiyan Wang, Yousheng Shu
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/27e43aacf71547879dfee2470702ea06
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spelling	oai:doaj.org-article:27e43aacf71547879dfee2470702ea062021-11-18T05:36:39ZEnhancement of asynchronous release from fast-spiking interneuron in human and rat epileptic neocortex.1544-91731545-788510.1371/journal.pbio.1001324https://doaj.org/article/27e43aacf71547879dfee2470702ea062012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22589699/?tool=EBIhttps://doaj.org/toc/1544-9173https://doaj.org/toc/1545-7885Down-regulation of GABAergic inhibition may result in the generation of epileptiform activities. Besides spike-triggered synchronous GABA release, changes in asynchronous release (AR) following high-frequency discharges may further regulate epileptiform activities. In brain slices obtained from surgically removed human neocortical tissues of patients with intractable epilepsy and brain tumor, we found that AR occurred at GABAergic output synapses of fast-spiking (FS) neurons and its strength depended on the type of connections, with FS autapses showing the strongest AR. In addition, we found that AR depended on residual Ca²⁺ at presynaptic terminals but was independent of postsynaptic firing. Furthermore, AR at FS autapses was markedly elevated in human epileptic tissue as compared to non-epileptic tissue. In a rat model of epilepsy, we found similar elevation of AR at both FS autapses and synapses onto excitatory neurons. Further experiments and analysis showed that AR elevation in epileptic tissue may result from an increase in action potential amplitude in the FS neurons and elevation of residual Ca²⁺ concentration. Together, these results revealed that GABAergic AR occurred at both human and rat neocortex, and its elevation in epileptic tissue may contribute to the regulation of epileptiform activities.Man JiangJie ZhuYaping LiuMingpo YangCuiping TianShan JiangYonghong WangHui GuoKaiyan WangYousheng ShuPublic Library of Science (PLoS)articleBiology (General)QH301-705.5ENPLoS Biology, Vol 10, Iss 5, p e1001324 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Biology (General) QH301-705.5
spellingShingle	Biology (General) QH301-705.5 Man Jiang Jie Zhu Yaping Liu Mingpo Yang Cuiping Tian Shan Jiang Yonghong Wang Hui Guo Kaiyan Wang Yousheng Shu Enhancement of asynchronous release from fast-spiking interneuron in human and rat epileptic neocortex.
description	Down-regulation of GABAergic inhibition may result in the generation of epileptiform activities. Besides spike-triggered synchronous GABA release, changes in asynchronous release (AR) following high-frequency discharges may further regulate epileptiform activities. In brain slices obtained from surgically removed human neocortical tissues of patients with intractable epilepsy and brain tumor, we found that AR occurred at GABAergic output synapses of fast-spiking (FS) neurons and its strength depended on the type of connections, with FS autapses showing the strongest AR. In addition, we found that AR depended on residual Ca²⁺ at presynaptic terminals but was independent of postsynaptic firing. Furthermore, AR at FS autapses was markedly elevated in human epileptic tissue as compared to non-epileptic tissue. In a rat model of epilepsy, we found similar elevation of AR at both FS autapses and synapses onto excitatory neurons. Further experiments and analysis showed that AR elevation in epileptic tissue may result from an increase in action potential amplitude in the FS neurons and elevation of residual Ca²⁺ concentration. Together, these results revealed that GABAergic AR occurred at both human and rat neocortex, and its elevation in epileptic tissue may contribute to the regulation of epileptiform activities.
format	article
author	Man Jiang Jie Zhu Yaping Liu Mingpo Yang Cuiping Tian Shan Jiang Yonghong Wang Hui Guo Kaiyan Wang Yousheng Shu
author_facet	Man Jiang Jie Zhu Yaping Liu Mingpo Yang Cuiping Tian Shan Jiang Yonghong Wang Hui Guo Kaiyan Wang Yousheng Shu
author_sort	Man Jiang
title	Enhancement of asynchronous release from fast-spiking interneuron in human and rat epileptic neocortex.
title_short	Enhancement of asynchronous release from fast-spiking interneuron in human and rat epileptic neocortex.
title_full	Enhancement of asynchronous release from fast-spiking interneuron in human and rat epileptic neocortex.
title_fullStr	Enhancement of asynchronous release from fast-spiking interneuron in human and rat epileptic neocortex.
title_full_unstemmed	Enhancement of asynchronous release from fast-spiking interneuron in human and rat epileptic neocortex.
title_sort	enhancement of asynchronous release from fast-spiking interneuron in human and rat epileptic neocortex.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/27e43aacf71547879dfee2470702ea06
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Enhancement of asynchronous release from fast-spiking interneuron in human and rat epileptic neocortex.

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