Kainic acid and seizure-induced Fos in subtypes of cerebrocortical neurons

被引:8
作者
Hiscock, JJ [1 ]
Mackenzie, L [1 ]
Medvedev, A [1 ]
Willoughby, JO [1 ]
机构
[1] Flinders Univ S Australia, Med Ctr, Dept Med, Adelaide, SA 5042, Australia
关键词
kainic acid; immunohistochemistry; calbindin D-28K; calretinin; parvalbumin; Fos;
D O I
10.1002/jnr.1252
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
Kainic acid injected in vivo into adult rats evokes the expression of the immediate early gene c-fos in the dentate gyrus and associated structures before a seizure occurs and in these and additional regions after a single motor seizure. The aim of this study was to identify cortical cell classes expressing Fos that correlate with these phenomena. Fos expression occurred before a seizure in the middle layers of entorhinal cortex in excitatory neurons and predominantly in calbindin D28-K-containing inhibitory neurons. Given the early Fos-labeling of these cells, we suggest they are associated with the hippocampal EEG events also seen at this stage of the effects of kainic acid, After a motor seizure Fos induction occurred in primary motor, sensory, piriform and entorhinal cortices, mainly in excitatory neurons, but also in a proportion of calcium binding protein-containing neurons proportionate to the degree of activation of the region as determined by Fos. Nearly 100% of neurons were Fos+ in entorhinal cortex, whereas 80% of excitatory and 50% of calcium binding protein-containing neurons were Fos+ in piriform cortex with lower proportions in neocortex. Of the calcium binding protein-containing neocortical neurons, calbindin D28-K cells exhibited the highest proportion of double labeling with Fos. This pattern of neocortical activation by kainic acid, a glutamate agonist, is only slightly different to that seen after seizures caused by blockade of gamma aminobutyric acid receptors suggesting that seizures caused by different mechanisms utilize similar neo-cortical circuitry. (C) 2001 Wiley-Liss, Inc.
引用
收藏
页码:1094 / 1100
页数:7
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