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Preconditioning with spreading depression activates specifically protein kinase Cdelta
1AI Virtanen Institute for Molecular Sciences, University of Kuopio, Finland.
Neuroreport
|February 24, 2001
Summary
Brief ischemia or spreading depression (SD) protects brain neurons from further injury. This study found that protein kinase C delta (PKCdelta) activation is key to this neuroprotection, showing increased levels and activity after preconditioning.
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- Preconditioning, using brief ischemia or spreading depression (SD), enhances neuronal tolerance to subsequent ischemic events.
- In the heart, similar preconditioning involves specific protein kinase C (PKC) isoforms (alpha, delta, epsilon, zeta).
Purpose of the Study:
- To investigate the role of PKC isoforms in neuronal tolerance induced by SD in the rat cortex.
- To analyze the temporal changes in PKCdelta expression, activity, and translocation following SD.
Main Methods:
- Spreading depression (SD) was induced in rat cortex via KCl application.
- Cortical tissues were analyzed at 30 minutes, 4 hours, and 12 hours post-SD.
- Protein levels, enzyme activity, membrane translocation, mRNA expression, and autophosphorylation of PKC isoforms were assessed.
Main Results:
- No significant changes in PKCalpha, epsilon, or zeta protein levels or activity were observed.
- A notable increase in PKCdelta membrane translocation occurred at 30 minutes and 12 hours post-SD.
- Late activation of PKCdelta, evidenced by increased mRNA, protein, and autophosphorylation at 12 hours, was confirmed.
Conclusions:
- PKCdelta plays a significant role in the neuroprotective mechanisms of preconditioning induced by spreading depression (SD).
- The late activation of PKCdelta suggests its involvement in the sustained tolerance conferred by preconditioning.