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The metabolic response to excitotoxicity - lessons from single-ce.pdf (1.7 MB)

The metabolic response to excitotoxicity - lessons from single-cell imaging.

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Version 2 2022-01-21, 09:07
Version 1 2019-11-22, 16:53
journal contribution
posted on 2019-11-22, 16:53 authored by Niamh M. Connolly, Jochen HM Prehn

Excitotoxicity is a pathological process implicated in neuronal death during ischaemia, traumatic brain injuries and neurodegenerative diseases. Excitotoxicity is caused by excess levels of glutamate and over-activation of NMDA or calcium-permeable AMPA receptors on neuronal membranes, leading to ionic influx, energetic stress and potential neuronal death. The metabolic response of neurons to excitotoxicity is complex and plays a key role in the ability of the neuron to adapt and recover from such an insult. Single-cell imaging is a powerful experimental technique that can be used to study the neuronal metabolic response to excitotoxicity in vitro and, increasingly, in vivo. Here, we review some of the knowledge of the neuronal metabolic response to excitotoxicity gained from in vitro single-cell imaging, including calcium and ATP dynamics and their effects on mitochondrial function, along with the contribution of glucose metabolism, oxidative stress and additional neuroprotective signalling mechanisms. Future work will combine knowledge gained from single-cell imaging with data from biochemical and computational techniques to garner holistic information about the metabolic response to excitotoxicity at the whole brain level and transfer this knowledge to a clinical setting.

Funding

Science Foundation Ireland (08/IN.1/B1949; 13/IA/1881)

History

Comments

This is a pre-print of an article published in Journal of Bioenergetics and Biomembranes. The final authenticated version is available online at: https://doi.org/10.1007/s10863-014-9578-4

Published Citation

Connolly NM, Prehn JH. The metabolic response to excitotoxicity - lessons from single-cell imaging. Journal of Bioenergetics and Biomembranes. 2015;47(1-2):75-88.

Publication Date

2015-04-01

Publisher

Springer Nature

PubMed ID

25262286