Parishin C's prevention of Aβ_1-42-induced inhibition of long-term potentiation is related to NMDA receptors

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• 作者：Zhihui Liu ; Weiping Wang ; Nan Feng ; Ling Wang ; Jiangong Shi ; Xiaoliang Wang ; ^{wangxl@imm.ac.cn" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Parishin C ; Long-term potentiation ; Neuroprotection ; NMDA receptors ; Ion channels
• 刊名：Acta Pharmaceutica Sinica B
• 出版年：2016
• 出版时间：May 2016
• 年：2016
• 卷：6
• 期：3
• 页码：189-197
• 全文大小：1270 K

文摘

The rhizome of Gastrodia elata (GE), a herb medicine, has been used for treatment of neuronal disorders in Eastern Asia for hundreds of years. Parishin C is a major ingredient of GE. In this study, the i.c.v. injection of soluble Aβ_1–42 oligomers model of LTP injury was used. We investigated the effects of parishin C on the improvement of LTP in soluble Aβ_1–42 oligomer–injected rats and the underlying electrophysiological mechanisms. Parishin C (i.p. or i.c.v.) significantly ameliorated LTP impairment induced by i.c.v. injection of soluble Aβ_1–42 oligomers. In cultured hippocampal neurons, soluble Aβ_1–42 oligomers significantly inhibited NMDAR currents while not affecting AMPAR currents and voltage-dependent currents. Pretreatment with parishin C protected NMDA receptor currents from the damage induced by Aβ. In summary, parishin C improved LTP deficits induced by soluble Aβ_1–42 oligomers. The protection by parishin C against Aβ-induced LTP damage might be related to NMDA receptors.