Gastrodin Suppresses the Amyloid β-Induced Increase of Spontaneous Discharge in the Entorhinal Cortex of Rats

Accumulated soluble amyloid beta- (Aβ-) induced aberrant neuronal network activity may directly contribute to cognitive deficits, which are the most outstanding characteristics of Alzheimer’s disease (AD). The entorhinal cortex (EC) is one of the earliest affected brain regions in AD. Impairments of...

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Main Authors: Peng-zhi Chen, Hui-hui Jiang, Bo Wen, Shuan-cheng Ren, Yang Chen, Wei-gang Ji, Bo Hu, Jun Zhang, Fenglian Xu, Zhi-ru Zhu
Format: Article
Language:English
Published: Wiley 2014-01-01
Series:Neural Plasticity
Online Access:http://dx.doi.org/10.1155/2014/320937
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author Peng-zhi Chen
Hui-hui Jiang
Bo Wen
Shuan-cheng Ren
Yang Chen
Wei-gang Ji
Bo Hu
Jun Zhang
Fenglian Xu
Zhi-ru Zhu
author_facet Peng-zhi Chen
Hui-hui Jiang
Bo Wen
Shuan-cheng Ren
Yang Chen
Wei-gang Ji
Bo Hu
Jun Zhang
Fenglian Xu
Zhi-ru Zhu
author_sort Peng-zhi Chen
collection DOAJ
description Accumulated soluble amyloid beta- (Aβ-) induced aberrant neuronal network activity may directly contribute to cognitive deficits, which are the most outstanding characteristics of Alzheimer’s disease (AD). The entorhinal cortex (EC) is one of the earliest affected brain regions in AD. Impairments of EC neurons are responsible for the cognitive deficits in AD. However, little effort has been made to investigate the effects of soluble Aβ on the discharge properties of EC neurons in vivo. The present study was designed to examine the effects of soluble Aβ1−42 on the discharge properties of EC neurons, using in vivo extracellular single unit recordings. The protective effects of gastrodin (GAS) were also investigated against Aβ1−42-induced alterations in EC neuronal activities. The results showed that the spontaneous discharge of EC neurons was increased by local application of soluble Aβ1−42 and that GAS can effectively reverse Aβ1−42-induced facilitation of spontaneous discharge in a concentration-dependent manner. Moreover, whole-cell patch clamp results indicated that the protective function of GAS on abnormal hyperexcitability may be partially mediated by its inhibitory action on Aβ1−42-elicited inward currents in EC neurons. Our study suggested that GAS may provide neuroprotective effects on Aβ1−42-induced hyperactivity in EC neurons of rats.
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spelling doaj-art-dd6ec7db919843b7b5c391c809f3071e2025-02-03T05:59:05ZengWileyNeural Plasticity2090-59041687-54432014-01-01201410.1155/2014/320937320937Gastrodin Suppresses the Amyloid β-Induced Increase of Spontaneous Discharge in the Entorhinal Cortex of RatsPeng-zhi Chen0Hui-hui Jiang1Bo Wen2Shuan-cheng Ren3Yang Chen4Wei-gang Ji5Bo Hu6Jun Zhang7Fenglian Xu8Zhi-ru Zhu9Department of Physiology, Third Military Medical University, Chongqing 400038, ChinaDepartment of Physiology, Third Military Medical University, Chongqing 400038, ChinaDepartment of Physiology, Third Military Medical University, Chongqing 400038, ChinaDepartment of Physiology, Third Military Medical University, Chongqing 400038, ChinaSchool of Acupuncture and Tuina, Chengdu University of Traditional Chinese Medicine, Chengdu 611130, ChinaDepartment of Chemistry, Third Military Medical University, Chongqing 400038, ChinaDepartment of Physiology, Third Military Medical University, Chongqing 400038, ChinaDepartment of Physiology, Third Military Medical University, Chongqing 400038, ChinaDepartment of Physiology and Pharmacology, The Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, T2N 4N1, CanadaDepartment of Physiology, Third Military Medical University, Chongqing 400038, ChinaAccumulated soluble amyloid beta- (Aβ-) induced aberrant neuronal network activity may directly contribute to cognitive deficits, which are the most outstanding characteristics of Alzheimer’s disease (AD). The entorhinal cortex (EC) is one of the earliest affected brain regions in AD. Impairments of EC neurons are responsible for the cognitive deficits in AD. However, little effort has been made to investigate the effects of soluble Aβ on the discharge properties of EC neurons in vivo. The present study was designed to examine the effects of soluble Aβ1−42 on the discharge properties of EC neurons, using in vivo extracellular single unit recordings. The protective effects of gastrodin (GAS) were also investigated against Aβ1−42-induced alterations in EC neuronal activities. The results showed that the spontaneous discharge of EC neurons was increased by local application of soluble Aβ1−42 and that GAS can effectively reverse Aβ1−42-induced facilitation of spontaneous discharge in a concentration-dependent manner. Moreover, whole-cell patch clamp results indicated that the protective function of GAS on abnormal hyperexcitability may be partially mediated by its inhibitory action on Aβ1−42-elicited inward currents in EC neurons. Our study suggested that GAS may provide neuroprotective effects on Aβ1−42-induced hyperactivity in EC neurons of rats.http://dx.doi.org/10.1155/2014/320937
spellingShingle Peng-zhi Chen
Hui-hui Jiang
Bo Wen
Shuan-cheng Ren
Yang Chen
Wei-gang Ji
Bo Hu
Jun Zhang
Fenglian Xu
Zhi-ru Zhu
Gastrodin Suppresses the Amyloid β-Induced Increase of Spontaneous Discharge in the Entorhinal Cortex of Rats
Neural Plasticity
title Gastrodin Suppresses the Amyloid β-Induced Increase of Spontaneous Discharge in the Entorhinal Cortex of Rats
title_full Gastrodin Suppresses the Amyloid β-Induced Increase of Spontaneous Discharge in the Entorhinal Cortex of Rats
title_fullStr Gastrodin Suppresses the Amyloid β-Induced Increase of Spontaneous Discharge in the Entorhinal Cortex of Rats
title_full_unstemmed Gastrodin Suppresses the Amyloid β-Induced Increase of Spontaneous Discharge in the Entorhinal Cortex of Rats
title_short Gastrodin Suppresses the Amyloid β-Induced Increase of Spontaneous Discharge in the Entorhinal Cortex of Rats
title_sort gastrodin suppresses the amyloid β induced increase of spontaneous discharge in the entorhinal cortex of rats
url http://dx.doi.org/10.1155/2014/320937
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