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Cited by 563Mitochondrial Function and PathologyCell death mechanisms and regulationPharmacological Receptor Mechanisms and Effects

Mitochondrial membrane potential and neuronal glutamate excitotoxicity: mortality and millivolts

Nicholls, David G., Ward, Manus W.·2000·Trends in Neurosciences
DOI 10.1016/s0166-2236(99)01534-9
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Abstract

In the past few years it has become apparent that mitochondria have an essential role in the life and death of neuronal and non-neuronal cells. The central mitochondrial bioenergetic parameter is the protonmotive force, Deltap. Much research has focused on the monitoring of the major component of Deltap, the mitochondrial membrane potential Deltapsim, in intact neurones exposed to excitotoxic stimuli, in the hope of establishing the causal relationships between cell death and mitochondrial dysfunction. Several fluorescent techniques have been used, and this article discusses their merits and pitfalls.

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Crossref · 10.1016/s0166-2236(99)01534-9

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  • The negative plasma membrane potential drives TPP+ movement from extracellular space into cytoplasm up to 10-fold, and TPP+ accumulates within mitochondria up to several hundred fold due to higher mitochondrial membrane potential.

    “This is achieved because the cells’ negative plasma membrane potential (-30mV to -60mV) drives the movement of TPP+ from the extracellular space into the cytoplasmic compartment up to 10-fold. TPP+ can further accumulate within the mitochondria up to several hundred fold due to the higher mitochondrial membrane potential (−140 to −180 mV) [15,16].”

    From Mitochondrially targeted compounds and their impact on cellular bioenergetics (2013) · cites this paper as [15]

  • Δψm influences reactive species generation and other critical mitochondrial functions, such as NAD reduction, ATP synthesis, and Ca+ sequestration, and is considered the primary dictator of mitochondrial energetics and an indicator of overall mitochondrial health in neurons.

    “Δψm not only influences RS generation but other critical mitochondrial functions, such as nicotinamide adenine dinucleotide reduction, ATP synthesis, and Ca+ sequestration, and is therefore considered the primary dictator of mitochondrial energetics as well as an indicator of the overall health of mitochondria in neurons (Nicholls and Ward, 2000).”

    From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Nicholls and Ward, 2000

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Authors
Nicholls, D. G., & Ward, M. W.
Affiliations
University of Dundee (GB)
ORCID
Venue
Trends in Neurosciences
Publisher
Elsevier BV
Published
2000-04
Volume
23
Issue
4
Pages
166-174
ISSN
0166-2236 (ISSN-L)
DOI
10.1016/s0166-2236(99)01534-9
OpenAlex
W2050297509
Cited by
563
References
1
Citations by year
2026: 7 · 2025: 8 · 2024: 13 · 2023: 16 · 2022: 8 · 2021: 19 · 2020: 18 · 2019: 20 · 2018: 23 · 2017: 26 · 2016: 20 · 2015: 18 · 2014: 26 · 2013: 20 · 2012: 22
FWCI
2.28
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Trends in Neurosciences (publishedVersion)
  • PubMed (publishedVersion)
Funders
Deutsche Forschungsgemeinschaft
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pharmacological Receptor Mechanisms and Effects
Keywords
mitochondrial membrane potential, glutamate excitotoxicity, neuronal cell death, proton motive force, mitochondrial dysfunction, fluorescent probes, neuronal bioenergetics
MeSH terms
Animals, Electrophysiology, Humans, Membrane Potentials, Membranes, Mitochondria, Neurons, Receptors, Glutamate, Excitatory Amino Acid Agonists

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