Please use this identifier to cite or link to this item: https://doi.org/10.1111/acel.12537
Title: Chelation of hippocampal zinc enhances long-term potentiation and synaptic tagging/capture in CA1 pyramidal neurons of aged rats: implications to aging and memory
Authors: Shetty, M.S 
Sharma, M 
Sajikumar, S 
Keywords: dopamine 1 receptor stimulating agent
zinc
chelating agent
dopamine receptor
dopamine receptor stimulating agent
n methyl dextro aspartic acid receptor
zinc
aging
animal tissue
Article
chelation
controlled study
enzyme activity
hippocampal CA1 region
long term potentiation
male
memory
nerve cell plasticity
nonhuman
priority journal
protein synthesis
pyramidal nerve cell
rat
synaptic transmission
aging
animal
cytology
drug effects
electrostimulation
hippocampal CA1 region
isolation and purification
long term potentiation
memory
metabolism
physiology
pyramidal nerve cell
synapse
Wistar rat
Aging
Animals
CA1 Region, Hippocampal
Chelating Agents
Dopamine Agonists
Electric Stimulation
Long-Term Potentiation
Male
Memory
Protein Biosynthesis
Pyramidal Cells
Rats, Wistar
Receptors, Dopamine
Receptors, N-Methyl-D-Aspartate
Synapses
Zinc
Issue Date: 2017
Publisher: Blackwell Publishing Ltd
Citation: Shetty, 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
Abstract: Aging 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.
Source Title: Aging Cell
URI: https://scholarbank.nus.edu.sg/handle/10635/173868
ISSN: 14749718
DOI: 10.1111/acel.12537
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