机构地区:[1]Department of Pathophysiology,Key Laboratory of the State Administration of Traditional Chinese Medicine,Medical College of Jinan University [2]GHM Institute of CNS Regeneration,Jinan University [3]Department of Orthopedics,First Affiliated Hospital,Medical College of Jinan University
出 处:《Neural Regeneration Research》2015年第6期925-931,共7页中国神经再生研究(英文版)
基 金:supported by the National Natural Science Foundation of China,No.81171134 and 81471235;a grant from the Introducing Talents of Discipline to Universities,No.B14036;a grant from the College Students’Extracurricular Scientific Innovation and Entrepreneurial Activity Research Topic of Jinan University Challenge Cup,No.(2013)27 and (2014)16;a grant from the College Students’Extracurricular Scientific Innovation and Entrepreneurial Activity Research Topic of Jinan University in China,No.201410559079,1055914162 and CX14261;a grant from the National Basic Research Program of China(973 Program),No.2011CB707501;the Science and Technology Foundation of Guangdong Province in China,No.2010B030700016;the Natural Science Foundation of Guangdong Province in China,No.2014A030313360
摘 要:Curcumin has been shown to significantly improve spatial memory impairment induced by HIV-1 gp 120 V3 in rats, but the electrophysiological mechanism remains unknown. Using extracellular microelectrode recording techniques, this study confirmed that the gp120 V3 loop could suppress long-term potentiation in the rat hippocampal CA1 region and synaptic plasticity, and that curcumin could antagonize these inhibitory effects. Using a Fura-2/AM calcium ion probe, we found that curcumin resisted the effects of the gp120 V3 loop on hippocampal synaptosomes and decreased Ca2+ concentration in synaptosomes. This effect of curcumin was identical to nimodipine, suggesting that curcumin improved the inhibitory effects of gpl20 on synaptic plasticity, ameliorated damage caused to the central nervous system, and might be a potential neuroprotective drug.Curcumin has been shown to significantly improve spatial memory impairment induced by HIV-1 gp 120 V3 in rats, but the electrophysiological mechanism remains unknown. Using extracellular microelectrode recording techniques, this study confirmed that the gp120 V3 loop could suppress long-term potentiation in the rat hippocampal CA1 region and synaptic plasticity, and that curcumin could antagonize these inhibitory effects. Using a Fura-2/AM calcium ion probe, we found that curcumin resisted the effects of the gp120 V3 loop on hippocampal synaptosomes and decreased Ca2+ concentration in synaptosomes. This effect of curcumin was identical to nimodipine, suggesting that curcumin improved the inhibitory effects of gpl20 on synaptic plasticity, ameliorated damage caused to the central nervous system, and might be a potential neuroprotective drug.
关 键 词:nerve regeneration CURCUMIN neurons HIV-1 gp l20 V3 loop plasticity HIV-associatedneurocognitive disorders output^input curve long-term potentiation excitatory postsynaptic potential paired-pulse facilitation Cd+ SYNAPTOSOME NSFC grants neural regeneration
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