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 Concept Videos

Drugs Affecting Neurotransmitter Synthesis01:29

Drugs Affecting Neurotransmitter Synthesis

2.0K
Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase,...
2.0K
Parkinson's Disease: Treatment01:24

Parkinson's Disease: Treatment

888
Neurodegenerative disorders, such as Parkinson's Disease (PD), involve the gradual and irreversible destruction of neurons in particular brain areas. These disorders exhibit standard features like proteinopathies, selective vulnerability of some neurons, and an interaction of intrinsic properties, genetics, and environmental influences in neural injury.
Parkinson's Disease is primarily a result of the loss of dopaminergic neurons in the substantia nigra pars compacta. The cornerstone of...
888
Anticholinesterase Agents: Poisoning and Treatment01:26

Anticholinesterase Agents: Poisoning and Treatment

1.4K
Anticholinesterases, also known as cholinesterase inhibitors, work by blocking the breakdown of acetylcholine, leading to its accumulation in the synaptic cleft. This accumulation indirectly enhances both muscarinic and nicotinic actions. These agents are classified as reversible or irreversible based on their mechanism of action.     
Irreversible agents form a strong bond with the cholinesterase enzyme, making it inactive. The breakdown of the phosphorylated enzyme is...
1.4K
Parkinson's Disease: Overview01:15

Parkinson's Disease: Overview

1.6K
Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is...
1.6K

You might also read

Related Articles

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

Sort by
Same author

<i>In vitro</i> evaluation of monoamine oxidase and acetylcholinesterase enzyme activities of <i>Capparis cartilaginea</i> Decne.

Natural product research·2026
Same author

Design, Synthesis, and Biological Evaluation of Novel Triazine-Based Dual Histone Deacetylase/phosphatidylinositol 3-kinase Inhibitors for Breast Cancer Therapy.

ChemMedChem·2026
Same author

MIF-Induced CD74+ Microglia and Macrophages Promote Progression of Brain Metastasis and Are Clinically Relevant across Central Nervous System Disorders.

Cancer research·2026
Same author

Metabolic thermodynamics: pertinent reference state and energy potentials.

The FEBS journal·2026
Same author

Breast Cancer Brain Metastases: Current Understanding and Future Directions.

Current oncology reports·2026
Same author

Response to Lehrer.

Journal of the National Cancer Institute·2026

Related Experiment Video

Updated: Dec 31, 2025

The 6-hydroxydopamine Rat Model of Parkinson's Disease
08:10

The 6-hydroxydopamine Rat Model of Parkinson's Disease

Published on: October 27, 2021

12.4K

6-Hydroxydopamine: a far from simple neurotoxin.

Damir Varešlija1,2, Keith F Tipton3, Gavin P Davey1

  • 1School of Biochemistry and Immunology, Trinity College, Dublin 2, Ireland.

Journal of Neural Transmission (Vienna, Austria : 1996)
|January 3, 2020
PubMed
Summary
This summary is machine-generated.

6-Hydroxydopamine (6-OHDA) is a neurotoxin used to model Parkinson's disease. Its breakdown generates toxic products and reactive oxygen species, contributing to its damaging effects on nerves.

Keywords:
4-HydroxynonenalAminochromeApoptosisAutoxidationDopamineHighly reactive oxygen species (hROS)Iron releaseMitochondriaNecrosisNeurotoxicityOxidative damageParkinson’s diseasePeroxynitriteReactive oxygen species (ROS)

More Related Videos

Development of a Unilaterally-lesioned 6-OHDA Mouse Model of Parkinson's Disease
10:09

Development of a Unilaterally-lesioned 6-OHDA Mouse Model of Parkinson's Disease

Published on: February 14, 2012

52.0K
Murine Model for Parkinson's Disease: from 6-OH Dopamine Lesion to Behavioral Test
08:06

Murine Model for Parkinson's Disease: from 6-OH Dopamine Lesion to Behavioral Test

Published on: January 15, 2010

32.3K

Related Experiment Videos

Last Updated: Dec 31, 2025

The 6-hydroxydopamine Rat Model of Parkinson's Disease
08:10

The 6-hydroxydopamine Rat Model of Parkinson's Disease

Published on: October 27, 2021

12.4K
Development of a Unilaterally-lesioned 6-OHDA Mouse Model of Parkinson's Disease
10:09

Development of a Unilaterally-lesioned 6-OHDA Mouse Model of Parkinson's Disease

Published on: February 14, 2012

52.0K
Murine Model for Parkinson's Disease: from 6-OH Dopamine Lesion to Behavioral Test
08:06

Murine Model for Parkinson's Disease: from 6-OH Dopamine Lesion to Behavioral Test

Published on: January 15, 2010

32.3K

Area of Science:

  • Neuroscience
  • Toxicology
  • Biochemistry

Background:

  • 6-Hydroxydopamine (6-OHDA) is a widely used neurotoxin.
  • It selectively destroys catecholaminergic nerves, serving as a model for Parkinson's disease in animal studies.
  • 6-OHDA undergoes autoxidation, producing toxic byproducts and reactive oxygen species.

Purpose of the Study:

  • To examine the mechanisms by which 6-OHDA induces neurotoxicity.
  • To investigate the role of its autoxidation products in cellular damage.
  • To understand the contribution of reactive oxygen species to 6-OHDA's effects.

Main Methods:

  • Review of existing literature on 6-OHDA neurotoxicity.
  • Analysis of the chemical properties and breakdown pathways of 6-OHDA.
  • Examination of the formation of harmful reactive oxygen species (hROS).

Main Results:

  • 6-OHDA rapidly autoxidizes, generating toxic compounds.
  • These products include reactive oxygen species (ROS).
  • 6-OHDA also facilitates the release of Fe(II), further promoting ROS formation.

Conclusions:

  • The toxic byproducts of 6-OHDA, including ROS, are key contributors to its neurotoxic effects.
  • Understanding these mechanisms is crucial for Parkinson's disease modeling.
  • Further research can explore targeted interventions against these toxic products.