Soluble Aβ oligomers impair hippocampal LTP by disrupting glutamatergic/GABAergic balance
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- 作者：Ming Leia ; b ; Huixin Xua ; Zhangyuan Lia ; Zemin Wanga ; Tiernan T. O'Malleya ; Dainan Zhanga ; Dominic M. Walsha ; Pingyi Xub ; c ; pingyixu@sina.com" class="auth_mail" title="E-mail the corresponding author ; Dennis J. Selkoea ; Shaomin Lia ; sli11@partners.org" class="auth_mail" title="E-mail the corresponding author
- 关键词：AD ; Alzheimer's disease ; oAβ ; soluble Aβ oligomers ; AP5 ; dl-2-amino-5-phosphonopentanoic acid ; fEPSP ; field excitatory postsynaptic potentials ; E&ndash ; S ; EPSP&ndash ; spike ; GT ; glutamate transporter ; IPSC ; inhibitory postsynaptic currents ; sEPSC ; spontaneous excitatory postsynaptic current ; PS ; population spike ; PTX ; picrotoxin ; TBOA ; dl-threo-β-benzyloxyaspartic acid
- 刊名：Neurobiology of Disease
- 出版年：2016
- 出版时间：January 2016
- 年：2016
- 卷：85
- 期：Complete
- 页码：111-121
- 全文大小：1765 K
文摘
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A glutamate uptake blocker occludes Aβ-mediated inhibition of E–S potentiation.
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Impairment of E–S potentiation by Aβ oligomers involves changes in GABAergic tone.
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Aβ oligomers increase both population spike frequency and spontaneous EPSC frequency.
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Decreasing neuronal activity prevents Aβ oligomer-impaired hippocampal LTP.
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Anticonvulsants restore Aβ oligomer-impaired hippocampal LTP.