%0 Journal Article
%T Chelation of hippocampal zinc enhances longİ\term potentiation and synaptic tagging/capture in CA1 pyramidal neurons of aged rats: implications to aging and memory
%A Mahima Sharma
%A Sreedharan Sajikumar
%J Archive of "Aging Cell".
%D 2017
%R 10.1111/acel.12537
%X 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 longİ\term associative memories, and a significant body of evidence shows that impairments in hippocampal function correlate with agingİ\related memory loss. A number of studies have implicated alterations in hippocampal synaptic plasticity, such as longİ\term potentiation (LTP), in ageİ\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 82İ\ to 84İ\weekİ\old male Wistar rats. We report increased zinc levels in the hippocampus of aged rats and also deficits in the tetaniİ\induced and dopaminergic agonistİ\induced lateİ\LTP and STC. The observed deficits in synaptic plasticity were restored upon chelation of zinc using a cellİ\permeable chelator. These data suggest that functional plasticity and associativity can be successfully established in aged neural networks by chelating zinc with cellİ\permeable chelating agents
%K aging
%K D1/D5 receptor
%K dopamine
%K longİ\term potentiation
%K synaptic tagging and capture
%K zinc
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5242293/