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Updated: Jul 6, 2026
10:36
Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
Published on: November 6, 2017
Calpain in the CNS: from synaptic function to neurotoxicity.
Jing Liu1, Ming Cheng Liu, Kevin K W Wang
1Center for Neuroproteomics and Biomarkers Research, Department of Psychiatry, McKnight Brain Institute, Post Office Box 100256, University of Florida, Gainesville, FL 32610, USA. jingl@ufl.edu
Science Signaling
|April 10, 2008
Summary
Calpains, calcium-activated proteases, have dual roles in the central nervous system (CNS). Their regulated activation is vital for synaptic function, while hyperactivation signals cellular damage and neurodegeneration.
Area of Science:
- Biochemistry
- Neuroscience
- Cell Biology
Background:
- Calpains are calcium-dependent cysteine proteases active at neutral pH.
- They exhibit two activation modes: controlled physiological activation and pathological hyperactivation during calcium overload.
Purpose of the Study:
- To elucidate the distinct roles of calpain activation in the central nervous system (CNS).
- To explore the potential of calpain cleavage products as biomarkers for neuronal injury and neurodegeneration.
Main Methods:
- The study discusses the biochemical properties and activation mechanisms of calpains.
- It reviews the substrates and physiological functions of calpains in the CNS.
- It examines the pathological implications of calpain hyperactivation.
Main Results:
- Regulated calpain activation in the CNS is crucial for synaptic function and memory formation.
- Substrates include structural proteins, enzymes, and glutamate receptors.
- Calpain hyperactivation is linked to severe cellular damage and neurodegenerative processes.
Conclusions:
- Calpain activity is critical for normal CNS function.
- Calpain cleavage products may serve as valuable biomarkers for detecting neurodegeneration and neuronal injury.
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