Related Experiment Video
Updated: Dec 29, 2025
07:33
A Simple Composite Phenotype Scoring System for Evaluating Mouse Models of Cerebellar Ataxia
Published on: May 21, 2010
37.0K
Cerebellar Ataxia Caused by Type II Unipolar Brush Cell Dysfunction in the Asic5 Knockout Mouse
Tabita Kreko-Pierce1, Nina Boiko1, Donald G Harbidge2
1Department of Cellular and Integrative Physiology, University of Texas Health Science Center at San Antonio, San Antonio, TX, 78299, USA.
Scientific Reports
|February 9, 2020
Summary
Deletion of acid-sensing ion channel 5 (Asic5) in unipolar brush cells (UBCs) impairs motor coordination. Loss of Asic5 alters UBC excitability and temporal processing, contributing to movement deficits.
Area of Science:
- Neuroscience
- Cellular Electrophysiology
- Motor Control
Background:
- Unipolar brush cells (UBCs) are key interneurons in the vestibulocerebellum.
- Acid-sensing ion channel 5 (Asic5) is highly expressed in type II UBCs.
Purpose of the Study:
- To investigate if Asic5 deletion causes ataxia.
- To elucidate the cellular mechanisms of ataxia in Asic5 knockout mice.
Main Methods:
- Assessed motor coordination and balance in Asic5 knockout mice.
- Utilized brain slice electrophysiology to study UBCs.
- Examined intrinsic UBC excitability and firing properties.
Main Results:
- Asic5 deletion impaired motor performance and balance.
- Reduced intrinsic UBC excitability and spontaneous action potential firing.
- Altered delayed hyperpolarizing K+ currents and burst firing frequency in UBCs.
Conclusions:
- Asic5 is crucial for normal type II UBC activity.
- Loss of Asic5 contributes to impaired movement and ataxia.
- Altered temporal processing of vestibular input in UBCs may underlie motor deficits.
