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The expression of Fos following kainic acid‐induced seizures is age‐dependent
Author(s) -
Silveira Diosely C.,
Sogawa Yoshimi,
Holmes Gregory L.
Publication year - 2002
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.0953-816x.2001.01849.x
Subject(s) - kainic acid , amygdala , limbic system , hippocampal formation , dentate gyrus , hippocampus , c fos , endocrinology , medicine , neuroscience , immediate early gene , psychology , chemistry , central nervous system , gene expression , glutamate receptor , receptor , biochemistry , gene
The expression of limbic seizures following kainic acid (KA) administration starts at approximately postnatal day (P) 19 in rats. In this study we investigated whether the expression of Fos‐like immunoreactivity (Fos‐IR) in limbic regions occurs concomitantly with the behavioural expression of limbic seizures. Immunohistochemistry for c‐Fos protein was examined 1, 2, 4, 12 and 24 h following seizure onset (KA‐treated rats) or saline injections (controls) in immature and adult rats at P7, P13, P20 and P60. The expression of Fos‐IR in limbic structures following KA‐induced seizures is age‐dependent. There is a strong and selective induction of Fos‐IR in the CA3 region of the hippocampus following KA‐induced seizures in rats at P7. However, the expression of Fos‐IR in KA‐treated rats at P13, P20 and P60 involved other hippocampal structures in addition to CA3. Abundant induction of Fos‐IR was found in the CA1, CA3 and dentate gyrus (DG) in KA‐treated rats at P13, P20 and P60. While immature rats at P7 and P13 showed very few or no Fos‐IR neurons in most amygdala nuclei, rat pups at P20 showed strong induction of Fos‐IR in the amygdala. Our results demonstrated that the induction of Fos‐IR in most amygdala nuclei and the full expression of behavioural limbic seizures occur at the same developmental age, which is consistent with the idea that the amygdala may play a role in the modulation of limbic seizures.

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