Processes enriched in neurons submitted to overstimulation by glutamate for 60 min and pathways related to and affected by excitotoxicity
Enriched process (glutamate overstimulation for 60 min) | Molecular mechanisms by affected by excitotoxicity |
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Protein localization at the membrane | Alterations in glutamate receptors (particularly NMDAR) and glutamate transporter functioning [9] |
Organelle transportation along microtubule and regulation of cellular component movement | Changes in Ca2+ buffering and transposition of mitochondria [87] |
Negative regulation of cellular amine metabolic | Over-recycling of glutamate in a dynamic pool, maintained through the glutamate-glutamine cycle by glutamine synthase in the cytoplasm of astrocytes and excitatory amino acid transporter dysfunction [88, 89] |
Response processes to axon injury | Degeneration of axons and dendrites by a process associated with excessive increases in [Ca2+]i and mitochondrial dysfunction [90] |
TG conceived the main hypothesis of the review. TG, JBS, GAJ, PNM, NT, LLP, LBM, DER, QY contributed to the manuscript writing and figures’ design. GAJ did the computational analysis. TG and JBS contributed to the formatting. TG, YT and HU reviewed the paper.
The authors declare that they have no conflicts of interest.
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HU acknowledges grant support from the São Paulo Research Foundation (FAPESP, Project Nos. 2018/07366-4 and 2018/08426-0) and the National Council for Scientific and Technological Development for fellowship support (CNPq, References Project No. 306392/2017-8). DER and TG are grateful for postdoctoral fellowships granted by FAPESP (Project Nos. 2018/17504-5 and 2015/13345-1-PD, respectively). LLP is grateful for a CNPq DTI-A fellowship (CNPq 380405/2020-2). The funders had no role in study design, data collection, and analysis, decision to publish, or preparation of the manuscript.
© The Author(s) 2022.