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

Abstract

<jats:title>Abstract</jats:title><jats:p>Kainic acid injected in vivo into adult rats evokes the expression of the immediate early gene <jats:italic>c‐fos</jats:italic> 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. J Neurosci. Res. 66:1094–1100, 2001. © 2001 Wiley‐Liss, Inc.</jats:p>