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

Monoamine-induced apoptotic neuronal cell death

R Zilkha-Falb1, I Ziv, N Nardi

  • 1Department of Neurobiochemistry, George S. Wise Faculty of Life Sciences, Tel Aviv University, Ramat Aviv, Israel.

Cellular and Molecular Neurobiology
|February 1, 1997
PubMed
Summary

All monoamines, including dopamine, norepinephrine, epinephrine, and serotonin, can trigger neuronal apoptosis. This programmed cell death mechanism may underlie neurodegenerative diseases like Parkinson's disease.

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

Clinical course and prognostic disparities of pyoderma gangrenosum based on underlying disease: A long-term comparative study in 124 patients.

Annales de dermatologie et de venereologie·2025
Same author

Exploring Remission Dynamics and Prognostic Factors in Lichen Planopilaris: A Retrospective Cohort Study.

Dermatology (Basel, Switzerland)·2024
Same author

Improved effectiveness of an increased dose of griseofulvin for treating Tinea capitis among refugee children in Israel: A retrospective cohort study.

Mycoses·2023
Same author

Percutaneous ethanol sclerotherapy is a promising treatment for recalcitrant angiolymphoid hyperplasia with eosinophilia.

Clinical and experimental dermatology·2021
Same author

Agminated benign vascular tumour successfully treated with trametinib.

The British journal of dermatology·2021
Same author

Exosomes derived from mesenchymal stem cells improved core symptoms of genetically modified mouse model of autism Shank3B.

Molecular autism·2020

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Monoamines (MA) like dopamine (DA), norepinephrine (NE), epinephrine (E), and serotonin (5-HT) are key neurotransmitters.
  • DA can induce apoptosis (programmed cell death) in neurons, suggesting a role in neurodegenerative diseases such as Parkinson's disease (PD).
  • PD also involves other MA systems, prompting investigation into their apoptotic potential.

Purpose of the Study:

  • To compare the apoptosis-triggering potential of NE, E, and 5-HT with DA.
  • To investigate MA-induced neuronal apoptosis in two distinct cell models: chick embryo sympathetic neurons and mouse cerebellar granule cells.

Main Methods:

  • Cultured postmitotic neurons (sympathetic and cerebellar granule cells) were treated with various monoamines.

Related Experiment Videos

  • Apoptosis was assessed via morphological changes (soma shrinkage, blebbing, nuclear fragmentation) and flow cytometry.
  • The role of antioxidants, transcription, and translation inhibitors was evaluated.

    • Main Results:

    • All tested MA induced neuronal apoptosis, characterized by distinct morphological and nuclear fragmentation patterns.
    • Cerebellar granule neurons were more sensitive to MA neurotoxicity than sympathetic neurons.
    • The potency of MA in inducing apoptosis followed the order: DA > NE ≈ E > 5-HT.
    • MA-induced apoptosis was blocked by antioxidants but not by transcription/translation inhibitors.

    Conclusions:

    • The apoptosis-triggering potential is a shared characteristic of all tested monoamines, likely mediated by oxidative metabolites.
    • Differential dose-dependencies and time courses of MA-induced apoptosis were observed.
    • Findings suggest a common underlying abnormality in neuronal apoptosis-control mechanisms across different monoaminergic systems, potentially relevant to PD pathogenesis.