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

You might also read

Related Articles

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

Sort by
Same author

Spatial memory deficits in mice induced by chemotherapeutic agents are prevented by acetylcholinesterase inhibitors.

Cancer chemotherapy and pharmacology·2019
Same author

Analysis of gait in rats with olivocerebellar lesions and ability of the nicotinic acetylcholine receptor agonist varenicline to attenuate impairments.

Behavioural brain research·2015
Same author

Gait analysis and the cumulative gait index (CGI): Translational tools to assess impairments exhibited by rats with olivocerebellar ataxia.

Behavioural brain research·2014
Same author

Neuronal nicotinic receptor agonists improve gait and balance in olivocerebellar ataxia.

Neuropharmacology·2013
Same author

A randomized trial of varenicline (Chantix) for the treatment of spinocerebellar ataxia type 3.

Neurology·2012
Same author

Nicotine-induced up regulation of α4β2 neuronal nicotinic receptors is mediated by the protein kinase C-dependent phosphorylation of α4 subunits.

Neuroscience·2010

Related Experiment Video

Updated: Mar 10, 2026

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease
08:09

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Published on: January 7, 2014

8.0K

3-Acetylpyridine neurotoxicity in mice.

L Wecker1, B Marrero-Rosado1, M E Engberg1

  • 1Department of Psychiatry and Behavioral Neurosciences, University of South Florida Morsani College of Medicine, Tampa, FL, United States.

Neurotoxicology
|December 18, 2016
PubMed
Summary

3-acetylpyridine (3-AP) causes neurotoxicity in mice, affecting balance and gait. Higher doses in mice, compared to rats, are needed to induce comparable motor deficits and neuronal loss in the inferior olive.

Keywords:
3-acetylpyridineAtaxiaBalanceGaitInferior oliveMouse

More Related Videos

Intracerebroventricular Treatment with Resiniferatoxin and Pain Tests in Mice
06:04

Intracerebroventricular Treatment with Resiniferatoxin and Pain Tests in Mice

Published on: September 2, 2020

9.0K
Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
08:01

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits

Published on: March 16, 2016

44.8K

Related Experiment Videos

Last Updated: Mar 10, 2026

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease
08:09

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Published on: January 7, 2014

8.0K
Intracerebroventricular Treatment with Resiniferatoxin and Pain Tests in Mice
06:04

Intracerebroventricular Treatment with Resiniferatoxin and Pain Tests in Mice

Published on: September 2, 2020

9.0K
Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
08:01

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits

Published on: March 16, 2016

44.8K

Area of Science:

  • Neuroscience
  • Animal Models
  • Motor Control

Background:

  • 3-acetylpyridine (3-AP) is a nicotinamide antagonist used to induce neurotoxicity.
  • 3-AP causes cerebellar ataxia in rats by damaging the inferior olive neurons.
  • Limited data exists on 3-AP's effects on mouse balance, gait, and its relationship to neuronal integrity.

Purpose of the Study:

  • To characterize the effects of 3-AP on balance and gait in mice.
  • To assess the impact of 3-AP on neuronal integrity in brain regions controlling motor coordination.
  • To elucidate the relationship between 3-AP-induced inferior olive lesions and behavioral deficits.

Main Methods:

  • Administration of 3-acetylpyridine to C57BL/6 mice.
  • Quantification of balance and gait alterations.
  • Assessment of neuronal loss (NeuN+ cells) in specific inferior olive subregions.
  • Correlation analysis between neuronal counts and rotorod performance.

Main Results:

  • C57BL/6 mice are less sensitive to 3-AP neurotoxicity than rats.
  • A dose 6.5 times higher than used in rats produced comparable balance and gait deficits.
  • Significant loss of NeuN+ neurons observed in multiple inferior olive subregions.
  • Neuronal counts in most studied subregions correlated significantly with rotorod performance.

Conclusions:

  • A specific high-dose regimen of 3-AP can effectively model ataxia in mice.
  • 3-AP-induced neuronal loss in the inferior olive is linked to motor behavior deficits.
  • This study provides a foundation for using 3-AP in mouse models of cerebellar dysfunction.