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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: Jiang, Man, Zhu, Jie, Liu, Yaping, Yang, Mingpo, Tian, Cuiping, Jiang, Shan, Wang, Yonghong, Guo, Hui, Wang, Kaiyan, Shu, Yousheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3348166/
https://www.ncbi.nlm.nih.gov/pubmed/22589699
http://dx.doi.org/10.1371/journal.pbio.1001324
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author Jiang, Man
Zhu, Jie
Liu, Yaping
Yang, Mingpo
Tian, Cuiping
Jiang, Shan
Wang, Yonghong
Guo, Hui
Wang, Kaiyan
Shu, Yousheng
author_facet Jiang, Man
Zhu, Jie
Liu, Yaping
Yang, Mingpo
Tian, Cuiping
Jiang, Shan
Wang, Yonghong
Guo, Hui
Wang, Kaiyan
Shu, Yousheng
author_sort Jiang, Man
collection PubMed
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 Ca(2+) 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 Ca(2+) 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.
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spelling pubmed-33481662012-05-15 Enhancement of Asynchronous Release from Fast-Spiking Interneuron in Human and Rat Epileptic Neocortex Jiang, Man Zhu, Jie Liu, Yaping Yang, Mingpo Tian, Cuiping Jiang, Shan Wang, Yonghong Guo, Hui Wang, Kaiyan Shu, Yousheng PLoS Biol Research Article 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 Ca(2+) 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 Ca(2+) 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. Public Library of Science 2012-05-08 /pmc/articles/PMC3348166/ /pubmed/22589699 http://dx.doi.org/10.1371/journal.pbio.1001324 Text en Jiang et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Jiang, Man
Zhu, Jie
Liu, Yaping
Yang, Mingpo
Tian, Cuiping
Jiang, Shan
Wang, Yonghong
Guo, Hui
Wang, Kaiyan
Shu, Yousheng
Enhancement of Asynchronous Release from Fast-Spiking Interneuron in Human and Rat Epileptic Neocortex
title 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_short 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
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3348166/
https://www.ncbi.nlm.nih.gov/pubmed/22589699
http://dx.doi.org/10.1371/journal.pbio.1001324
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