Please use this identifier to cite or link to this item: https://doi.org/10.1111/acel.12537
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dc.titleChelation of hippocampal zinc enhances long-term potentiation and synaptic tagging/capture in CA1 pyramidal neurons of aged rats: implications to aging and memory
dc.contributor.authorShetty, M.S
dc.contributor.authorSharma, M
dc.contributor.authorSajikumar, S
dc.date.accessioned2020-09-01T08:01:20Z
dc.date.available2020-09-01T08:01:20Z
dc.date.issued2017
dc.identifier.citationShetty, M.S, Sharma, M, Sajikumar, S (2017). Chelation of hippocampal zinc enhances long-term potentiation and synaptic tagging/capture in CA1 pyramidal neurons of aged rats: implications to aging and memory. Aging Cell 16 (1) : 136-148. ScholarBank@NUS Repository. https://doi.org/10.1111/acel.12537
dc.identifier.issn14749718
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/173868
dc.description.abstractAging is associated with decline in cognitive functions, prominently in the memory consolidation and association capabilities. Hippocampus plays a crucial role in the formation and maintenance of long-term associative memories, and a significant body of evidence shows that impairments in hippocampal function correlate with aging-related memory loss. A number of studies have implicated alterations in hippocampal synaptic plasticity, such as long-term potentiation (LTP), in age-related cognitive decline although exact mechanisms underlying are not completely clear. Zinc deficiency and the resultant adverse effects on cognition have been well studied. However, the role of excess of zinc in synaptic plasticity, especially in aging, is not addressed well. Here, we have investigated the hippocampal zinc levels and the impairments in synaptic plasticity, such as LTP and synaptic tagging and capture (STC), in the CA1 region of acute hippocampal slices from 82- to 84-week-old male Wistar rats. We report increased zinc levels in the hippocampus of aged rats and also deficits in the tetani-induced and dopaminergic agonist-induced late-LTP and STC. The observed deficits in synaptic plasticity were restored upon chelation of zinc using a cell-permeable chelator. These data suggest that functional plasticity and associativity can be successfully established in aged neural networks by chelating zinc with cell-permeable chelating agents. © 2016 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
dc.publisherBlackwell Publishing Ltd
dc.sourceUnpaywall 20200831
dc.subjectdopamine 1 receptor stimulating agent
dc.subjectzinc
dc.subjectchelating agent
dc.subjectdopamine receptor
dc.subjectdopamine receptor stimulating agent
dc.subjectn methyl dextro aspartic acid receptor
dc.subjectzinc
dc.subjectaging
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectchelation
dc.subjectcontrolled study
dc.subjectenzyme activity
dc.subjecthippocampal CA1 region
dc.subjectlong term potentiation
dc.subjectmale
dc.subjectmemory
dc.subjectnerve cell plasticity
dc.subjectnonhuman
dc.subjectpriority journal
dc.subjectprotein synthesis
dc.subjectpyramidal nerve cell
dc.subjectrat
dc.subjectsynaptic transmission
dc.subjectaging
dc.subjectanimal
dc.subjectcytology
dc.subjectdrug effects
dc.subjectelectrostimulation
dc.subjecthippocampal CA1 region
dc.subjectisolation and purification
dc.subjectlong term potentiation
dc.subjectmemory
dc.subjectmetabolism
dc.subjectphysiology
dc.subjectpyramidal nerve cell
dc.subjectsynapse
dc.subjectWistar rat
dc.subjectAging
dc.subjectAnimals
dc.subjectCA1 Region, Hippocampal
dc.subjectChelating Agents
dc.subjectDopamine Agonists
dc.subjectElectric Stimulation
dc.subjectLong-Term Potentiation
dc.subjectMale
dc.subjectMemory
dc.subjectProtein Biosynthesis
dc.subjectPyramidal Cells
dc.subjectRats, Wistar
dc.subjectReceptors, Dopamine
dc.subjectReceptors, N-Methyl-D-Aspartate
dc.subjectSynapses
dc.subjectZinc
dc.typeArticle
dc.contributor.departmentPHYSIOLOGY
dc.description.doi10.1111/acel.12537
dc.description.sourcetitleAging Cell
dc.description.volume16
dc.description.issue1
dc.description.page136-148
dc.published.statePublished
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