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. Impairmen...

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Veröffentlicht in:Neural plasticity. - 1998. - 2014(2014) vom: 26., Seite 320937
1. Verfasser: Chen, Peng-zhi (VerfasserIn)
Weitere Verfasser: Jiang, Hui-hui, Wen, Bo, Ren, Shuan-cheng, Chen, Yang, Ji, Wei-gang, Hu, Bo, Zhang, Jun, Xu, Fenglian, Zhu, Zhi-ru
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2014
Zugriff auf das übergeordnete Werk:Neural plasticity
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Amyloid beta-Peptides Benzyl Alcohols Glucosides Neuroprotective Agents Peptide Fragments amyloid beta-protein (1-42) gastrodin 5YS9U2W3RQ
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520 |a 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 Aβ(1-42) on the discharge properties of EC neurons, using in vivo extracellular single unit recordings. The protective effects of gastrodin (GAS) were also investigated against Aβ(1-42)-induced alterations in EC neuronal activities. The results showed that the spontaneous discharge of EC neurons was increased by local application of soluble Aβ(1-42) and that GAS can effectively reverse Aβ(1-42)-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 Aβ(1-42)-elicited inward currents in EC neurons. Our study suggested that GAS may provide neuroprotective effects on Aβ(1-42)-induced hyperactivity in EC neurons of rats 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 7 |a Amyloid beta-Peptides  |2 NLM 
650 7 |a Benzyl Alcohols  |2 NLM 
650 7 |a Glucosides  |2 NLM 
650 7 |a Neuroprotective Agents  |2 NLM 
650 7 |a Peptide Fragments  |2 NLM 
650 7 |a amyloid beta-protein (1-42)  |2 NLM 
650 7 |a gastrodin  |2 NLM 
650 7 |a 5YS9U2W3RQ  |2 NLM 
700 1 |a Jiang, Hui-hui  |e verfasserin  |4 aut 
700 1 |a Wen, Bo  |e verfasserin  |4 aut 
700 1 |a Ren, Shuan-cheng  |e verfasserin  |4 aut 
700 1 |a Chen, Yang  |e verfasserin  |4 aut 
700 1 |a Ji, Wei-gang  |e verfasserin  |4 aut 
700 1 |a Hu, Bo  |e verfasserin  |4 aut 
700 1 |a Zhang, Jun  |e verfasserin  |4 aut 
700 1 |a Xu, Fenglian  |e verfasserin  |4 aut 
700 1 |a Zhu, Zhi-ru  |e verfasserin  |4 aut 
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