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Published on: March 11, 2020
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m-Calpain is released from striatal synaptosomes.
Nina Pestereva1, Irina Ivleva1, Alexander Zubov1
1Department of Physiology (Pavlov's), Institute of Experimental Medicine, St. Petersburg, Russia.
The International Journal of Neuroscience
|March 10, 2021
Summary
Active m-calpain, a calcium-dependent protease, is released from synaptosomes. This release, which is not due to synaptosome damage, can be blocked by glyburide, an ABC transporter inhibitor.
Area of Science:
- Neuroscience
- Biochemistry
Background:
- Synaptosomes are crucial for neurotransmission.
- Calpains are calcium-dependent proteases involved in cellular processes.
Purpose of the Study:
- To investigate the release of m-calpain (a calcium-dependent neutral cysteine protease) from synaptosomes.
- To determine if this release is linked to synaptosome integrity.
- To explore potential mechanisms and inhibitors of m-calpain release.
Main Methods:
- Wistar rat synaptosomes were isolated and their integrity assessed using LDH activity.
- Calpain activity was measured via casein zymography.
- Extracellular calpain was detected using immunoprecipitation and immunoblotting.
- Secretion prediction tools (PrediSi, SecretomeP) were employed to analyze nonclassical secretion pathways.
Main Results:
- Calcium- and time-dependent release of active or activatable m-calpain from synaptosomes was demonstrated, independent of synaptosome integrity.
- Computational analysis indicated a high probability for the nonclassical secretion of rat m-calpain.
- The release of m-calpain was significantly suppressed by glyburide, an ABC transporter inhibitor.
- Potential extracellular calpain substrates, including matrix metalloproteinases and alpha-synuclein, were identified.
Conclusions:
- Active m-calpain is present in the extracellular medium of striatal synaptosomes.
- Glyburide effectively prevents the release of m-calpain from synaptosomes.
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