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J Korean Neurosurg Soc. 1998 Dec;27(12):1641-1652. Korean. Original Article.
Lee JK , Kang SS , Lee MC .
Department of Neurosurgery, Chonnam National University Medical School, Kwangju, Korea.
Department of Pathology, Chonnam National University Medical School, Kwangju, Korea.

To investigate neuronal injury developed in an experimental model of temporal lobe epilepsy, the expression of c-FOS, c-JUN and HSP72 on the amygdala, hippocampus and temporal neocortex was studied. Epileptic seizure was induced in rats by microinjection of kainic acid(1microgrm/microl) dissolved in phosphate buffer(0.1 M, pH 7.4) into the left amygdala. Selective and delayed neuronal injuries appeared in the CA3 region of the hippocampus after 14 days and were characterized by swelling of cytoplasm and neurites, nuclear pyknosis and loss of neurons. Early induction of c-FOS and c-JUN was noted on the injection-side amygdala at 1-12h, and delayed expression developed at 7 days after the injection. HSP72 expression appeared continuously 3 hrs after the injection. Delayed induction of c-FOS, c-JUN and continuous expression of HSP72 were observed in the hippocampus and entorhinal cortex. In the hippocampus, c-FOS expression was relatively strong in the neurons of CA3 and dentate gyrus at 7~14 days after the injection. Similar findings were also noted in the neurons of the entorhinal cortex. Induction of HSP72 occurred slightly later than on that of c-FOS and c-JUN in the amygdala, with the prominent induction being noted in the neurons of amygdala, CA2, CA3, CA4 and dentate gyrus at 3 to 21 days after the injection. These results suggested that the delayed expressions of c-FOS and c-JUN in the hippocampus correlated well with impending clinical epileptic seizure.

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