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Long-lasting decreases of type II calmodulin kinase expression in kindled rat brains
J M Bronstein1, P Micevych, P Popper
1Department of Neurology, UCLA School of Medicine 90024.
Abstract:
The kindling model of epilepsy is associated with long-lasting changes in type II calmodulin kinase (CaM kinase) activity and immunoreactivity. In order to determine the mechanism of these alterations, we measured gene expression of CaM kinase using in situ hybridization in septally kindled rat brains and paired controls using a 35S-labeled riboprobe for the beta subunit of the enzyme. We found CaM kinase mRNA concentrated in the hippocampus and other limbic structures. Kindling decreased hippocampal CaM kinase mRNA by 30% in CA1, 34% in CA2, 35% in CA3 41% in CA4, and 29% in the dentate gyrus. Hybridization was also decreased by 21% in the cerebral cortex but not in the lateral septum. These changes are similar in distribution and direction to those previously measured by immunohistochemistry. These data suggest that altered CaM kinase activity and immunoreactivity associated with kindling reflect long-lasting alterations in gene expression of this important synaptic protein, and provide further evidence for its possible importance in the kindling phenomenon.
Insights
Kindling epilepsy causes long-lasting changes in CaM kinase gene expression, particularly in the hippocampus. This suggests altered gene expression underlies the observed changes in CaM kinase activity and its role in epilepsy.
Area of Science:
- Neuroscience
- Molecular Biology
- Epilepsy Research
Background:
- The kindling model of epilepsy is characterized by persistent alterations in type II calmodulin kinase (CaM kinase) activity and immunoreactivity.
- Understanding the molecular mechanisms behind these changes is crucial for epilepsy research.
Purpose of the Study:
- To investigate the mechanism behind long-lasting changes in CaM kinase in the kindling model of epilepsy.
- To measure CaM kinase gene expression in the brains of rats subjected to septal kindling.
Main Methods:
- Utilized in situ hybridization with a 35S-labeled riboprobe to quantify CaM kinase mRNA (beta subunit).
- Examined gene expression in septally kindled rat brains and compared them to control groups.
- Analyzed hybridization signals in various brain regions, including the hippocampus, cerebral cortex, and lateral septum.
Main Results:
- CaM kinase mRNA was found to be concentrated in the hippocampus and other limbic structures.
- Kindling significantly decreased hippocampal CaM kinase mRNA levels across all subfields (CA1-CA4, dentate gyrus) by 29-41%.
- A 21% decrease in CaM kinase mRNA was observed in the cerebral cortex, with no significant change in the lateral septum.
Conclusions:
- Altered CaM kinase activity and immunoreactivity in kindling epilepsy are linked to long-lasting changes in gene expression.
- These findings support the role of CaM kinase gene expression alterations in the kindling phenomenon.
- Provides evidence for CaM kinase's importance as a synaptic protein in the context of epilepsy.