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Inhibition of AMPAR endocytosis alleviates pentobarbital-induced spatial memory deficits and synaptic depression.
Behav Brain Res. 2018 Feb 26; 339:66-72.BB

Abstract

Our previous study has shown that pentobarbital causes memory deficits and impairs hippocampal synaptic plasticity. The Tat-GluA23Y peptide (GluA23Y) prevents activity-dependent α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) endocytosis. It enables early-phase long-term potentiation (LTP) to proceed to late-phase LTP allowing short-term memory to convert to long-term memory. The purpose of this study is to explore the potential effects of GluA23Y on pentobarbital-induced memory deficits through behavioral and electrophysiological paradigms. We found that in vivo intrahippocampal infusion of GluA23Y (100μM, 1μl per hippocampus) 30min prior to pentobarbital administration (8mM, 1μl per hippocampus) significantly rescued the pentobarbital-induced deficit of memory retrieval in rats during the Morris water maze test. Pre-incubation of GluA23Y (10μM) partially rescued bath application of pentobarbital-induced synaptic transmission of the CA3-CA1 pathway in hippocampal slices. More importantly, GluA23Y selectively upregulated the synaptic GluA2 expression that was suppressed by pentobarbital. Together, these results suggest that inhibition of GluA2-containing AMPAR endocytosis by GluA23Y increases the pentobarbital-suppressed basal synaptic transmission by upregulating the synaptic GluA2, and then subsequently alleviates spatial memory deficits. Therefore, inhibition of AMPAR endocytosis may be a potential therapeutic way to treat memory disorders caused by anesthetics.

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Authors+Show Affiliations

Wang W
Ministry of Education Key Laboratory of Child Development and Disorders and Chongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Tan T
Ministry of Education Key Laboratory of Child Development and Disorders and Chongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Yu Y
Ministry of Education Key Laboratory of Child Development and Disorders and Chongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Huang Z
Ministry of Education Key Laboratory of Child Development and Disorders and Chongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Du Y
Ministry of Education Key Laboratory of Child Development and Disorders and Chongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Han H
Ministry of Education Key Laboratory of Child Development and Disorders and Chongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Dong Z
Ministry of Education Key Laboratory of Child Development and Disorders and Chongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China. Electronic address: zfdong@aliyun.com.

MeSH

AnimalsDepressionEndocytosisHippocampusLong-Term PotentiationMaleMemory DisordersMemory, Long-TermNeuronal PlasticityPentobarbitalRats, Sprague-DawleySynaptic Transmission

Pub Type(s)

Journal Article

Language

eng

PubMed ID

29162383

Citation

Wang, Wei, et al. "Inhibition of AMPAR Endocytosis Alleviates Pentobarbital-induced Spatial Memory Deficits and Synaptic Depression." Behavioural Brain Research, vol. 339, 2018, pp. 66-72.
Wang W, Tan T, Yu Y, et al. Inhibition of AMPAR endocytosis alleviates pentobarbital-induced spatial memory deficits and synaptic depression. Behav Brain Res. 2018;339:66-72.
Wang, W., Tan, T., Yu, Y., Huang, Z., Du, Y., Han, H., & Dong, Z. (2018). Inhibition of AMPAR endocytosis alleviates pentobarbital-induced spatial memory deficits and synaptic depression. Behavioural Brain Research, 339, 66-72. https://doi.org/10.1016/j.bbr.2017.11.020
Wang W, et al. Inhibition of AMPAR Endocytosis Alleviates Pentobarbital-induced Spatial Memory Deficits and Synaptic Depression. Behav Brain Res. 2018 Feb 26;339:66-72. PubMed PMID: 29162383.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibition of AMPAR endocytosis alleviates pentobarbital-induced spatial memory deficits and synaptic depression. AU - Wang,Wei, AU - Tan,Tao, AU - Yu,Yanzhi, AU - Huang,Zhilin, AU - Du,Yehong, AU - Han,Huili, AU - Dong,Zhifang, Y1 - 2017/11/21/ PY - 2017/10/05/received PY - 2017/11/09/revised PY - 2017/11/16/accepted PY - 2017/11/23/pubmed PY - 2018/8/8/medline PY - 2017/11/23/entrez KW - AMPAR endocytosis KW - Pentobarbital KW - Spatial memory retrieval KW - Synaptic depression SP - 66 EP - 72 JF - Behavioural brain research JO - Behav Brain Res VL - 339 N2 - Our previous study has shown that pentobarbital causes memory deficits and impairs hippocampal synaptic plasticity. The Tat-GluA23Y peptide (GluA23Y) prevents activity-dependent α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) endocytosis. It enables early-phase long-term potentiation (LTP) to proceed to late-phase LTP allowing short-term memory to convert to long-term memory. The purpose of this study is to explore the potential effects of GluA23Y on pentobarbital-induced memory deficits through behavioral and electrophysiological paradigms. We found that in vivo intrahippocampal infusion of GluA23Y (100μM, 1μl per hippocampus) 30min prior to pentobarbital administration (8mM, 1μl per hippocampus) significantly rescued the pentobarbital-induced deficit of memory retrieval in rats during the Morris water maze test. Pre-incubation of GluA23Y (10μM) partially rescued bath application of pentobarbital-induced synaptic transmission of the CA3-CA1 pathway in hippocampal slices. More importantly, GluA23Y selectively upregulated the synaptic GluA2 expression that was suppressed by pentobarbital. Together, these results suggest that inhibition of GluA2-containing AMPAR endocytosis by GluA23Y increases the pentobarbital-suppressed basal synaptic transmission by upregulating the synaptic GluA2, and then subsequently alleviates spatial memory deficits. Therefore, inhibition of AMPAR endocytosis may be a potential therapeutic way to treat memory disorders caused by anesthetics. SN - 1872-7549 UR - https://www.unboundmedicine.com/medline/citation/29162383/Inhibition_of_AMPAR_endocytosis_alleviates_pentobarbital_induced_spatial_memory_deficits_and_synaptic_depression_ DB - PRIME DP - Unbound Medicine ER -