Regulation of neuronal excitability by reactive oxygen species and calcium signaling: Insights into brain aging
Altered cognition and inefficient learning and memory are hallmarks of brain aging resulting from many small changes in the structure and function of neurons. One such change is a decrease in excitatory synaptic transmission mediated by glutamate and its binding to the AMPA and NMDA subtypes of glut...
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Published in | Current research in neurobiology Vol. 2; p. 100012 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Elsevier B.V
2021
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | Altered cognition and inefficient learning and memory are hallmarks of brain aging resulting from many small changes in the structure and function of neurons. One such change is a decrease in excitatory synaptic transmission mediated by glutamate and its binding to the AMPA and NMDA subtypes of glutamate receptors. Why there is decreased glutamatergic transmission in aging is not well understood. Interestingly, in aged excitatory neurons, abnormal calcium homeostasis and energy production are reliably observed. These processes have also been shown to modulate the transport and delivery of glutamate receptors to synapses. Most of these channels are translated in the cell body and must be transported to synapses by molecular motors and then transferred to the synaptic surface for proper function. Despite there being little to no research on how aging impacts these transport processes, a detailed understanding of the mechanisms regulating long-distance and local transport of these channels is coming together. Here, we review recent research on how synaptic content, specifically of glutamate receptors and voltage-gated calcium channels, is normally regulated by calcium and energy production. In addition, we discuss how that regulation may change in the aged nervous system. These advances begin to detail a mechanistic explanation in which an interplay between calcium signaling and metabolism are impacted by and, in-turn, regulate the strength of excitatory synapses.
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•Calcium signaling is central to glutamatergic synapse maintenance and plasticity.•Reactive oxygen species bidirectionally modulate calcium levels at physiological states.•Many neuronal mechanisms are co-regulated by oxidation and calcium signaling.•New research on this co-regulation is insightful for physiological neuronal aging. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 2665-945X 2665-945X |
DOI: | 10.1016/j.crneur.2021.100012 |