Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Mitochondrial dysfunction and dendritic beading during neuronal toxicity.

Sam M Greenwood1, Sarah M Mizielinska, Bruno G Frenguelli

  • 1Neurosciences Institute, Ninewells Medical School, University of Dundee, Dundee DD19SY, Scotland, United Kingdom.

The Journal of Biological Chemistry
|July 10, 2007
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Therapeutic Potential of Leptin in Neurodegenerative Disease.

Biomedicines·2025
Same author

Transient Single Cell Hypoxia Induced by Localized Galvanostatic Oxygen Challenge.

ACS measurement science au·2025
Same author

Soluble tau aggregates decrease the threshold for thalamic oscillations and increase the excitability of thalamic neurons.

Neuropharmacology·2025
Same author

A term as Editor-in-Chief of Neuropharmacology: Ups and downs and highs and lows.

Neuropharmacology·2024
Same author

MSK1 is required for the experience- and ampakine-dependent enhancement of spatial reference memory and reversal learning and for the induction of Arc and BDNF.

Neuropharmacology·2024
Same author

Novel Leptin-Based Therapeutic Strategies to Limit Synaptic Dysfunction in Alzheimer's Disease.

International journal of molecular sciences·2024
Same journal

Correction: Characterization of Mast2 kinase defines structural features, regulation, and substrates.

The Journal of biological chemistry·2026
Same journal

Isotope-Edited ESEEM: A New Method for Probing Copper Binding Sites in Neurodegenerative Proteins.

The Journal of biological chemistry·2026
Same journal

Introduction to the Thematic Review Series on Intracellular Protein Degradation. The ubiquitous biology of intracellular protein degradation: a tribute to Alfred L. ("Fred") Goldberg.

The Journal of biological chemistry·2026
Same journal

Correction: Aromatic residue-rich amino-terminal segments of temporin L self-assemble into collagen-mimetic peptides with cell-adhesion properties.

The Journal of biological chemistry·2026
Same journal

YhbO is a DJ-1 family glyoxalase and α-oxoaldehyde hydratase that confers resistance to reactive carbonyl stress (112).

The Journal of biological chemistry·2026
Same journal

ARMH3 acts as a central scaffold at the Golgi/TGN through interactions with Arl5, GBF1, and PI4KB.

The Journal of biological chemistry·2026
See all related articles

Mitochondrial dysfunction and dendritic beading are linked in neuronal damage. Recovery depends on mitochondrial membrane potential, not ATP levels, suggesting a key role for mitochondria in neuronal resilience.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Neuronal toxicity involves mitochondrial dysfunction, ATP depletion, and neuritic beading.
  • These events are observed in various pathological conditions affecting neurons.

Purpose of the Study:

  • To investigate the spatiotemporal relationship between mitochondrial dysfunction and dendritic beading.
  • To elucidate the roles of mitochondrial depolarization and ATP depletion in inducing these morphological changes.
  • To understand the mechanisms underlying dendritic recovery after neurotoxic insult.

Main Methods:

  • Inducing neuronal toxicity using glutamate exposure and oxygen-glucose deprivation.
  • Observing mitochondrial changes (depolarization, collapse) and dendritic beading.

Related Experiment Videos

  • Analyzing the temporal sequence and spatial propagation of these events.
  • Assessing the impact of mitochondrial membrane potential and ATP levels on dendritic recovery.

    • Main Results:

    • Mitochondrial depolarization and collapse precede dendritic beading during oxygen-glucose deprivation.
    • These events propagate as a wave from dendrites to the cell body.
    • Mitochondrial depolarization and ATP depletion do not directly trigger beading but increase vulnerability.
    • Dendritic recovery is dependent on mitochondrial membrane potential integrity, not ATP synthesis.

    Conclusions:

    • Glutamate excitotoxicity involves Ca(2+) influx causing mitochondrial depolarization and Na(+) influx driving ATP depletion.
    • This cascade leads to dendritic beading, with mitochondrial dysfunction increasing susceptibility.
    • Dendritic recovery is contingent on maintaining mitochondrial membrane potential, highlighting its crucial role in neuronal resilience.