J Korean Med Sci.  2001 Oct;16(5):643-648. 10.3346/jkms.2001.16.5.643.

Calcium/Calmodulin Kinase II Activity of Hippocampus in Kainate-Induced Epilepsy

• Lee MC
• Ban SS
• Woo YJ
• Kim SU

• KMID: 2157576
• DOI: http://doi.org/10.3346/jkms.2001.16.5.643

Abstract

This study investigated calcium/calmodulin kinase II (CaMKII) activity related to long-standing neuronal injury of the hippocampus in kainate (KA)-induced experimental temporal lobe epilepsy. Epileptic seizure was induced by injection of KA (1 g/L) dissolved in phosphate buffer (0.1 M, pH 7.4) into the left amygdala. Clinical seizures, histopathologic changes and CaMKII activity of the hippocampus were evaluated. Characteristic early limbic and late seizures were developed. Hippocampal CaMKII activity increased significantly 4 and 8 weeks after intra-amygdaloid injection of KA, when late seizures developed. The histopathologic changes of the hippocampus included swelling of neuronal cytoplasm with nuclear pyknosis and loss of neurons in CA3 during this period. The increased activity of CaMKII may correlate with appearance of distant damage in the hippocampus. The above results indicate that intra-amygdaloid injection of KA produces excitatory signals for ipsilateral CA3 neurons in the hippocampus and that subsequently increased levels of CaMKII in postsynaptic neurons induce neuronal injury via phosphorylation of N-methyl-D-aspartate type glutamate receptor.

Keyword

Ca(2+)-Calmodulin Dependent Protein Kinase; Epilepsy; Hippocampus; Kainic Acid; Neurons

MeSH Terms

Animal
Ca(2+)-Calmodulin Dependent Protein Kinase/*metabolism
Epilepsy, Temporal Lobe/chemically induced/*enzymology/pathology
Hippocampus/*enzymology/pathology
Kainic Acid/*toxicity
Long-Term Potentiation/drug effects
Male
Rats
Rats, Wistar