Kainic acid and seizure-induced Fos in subtypes of cerebrocortical neurons.
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.
Hiscock
J J
JJ
Department of Medicine, Medical Centre, Flinders University of South Australia, G.P.O. Box 2100, Adelaide S.A. 5042, Australia.
Mackenzie
L
L
Medvedev
A
A
Willoughby
J O
JO
D000818:Animals; D002135:Calcium-Binding Proteins / Q000187:drug effects / Q000378:metabolism*; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D018728:Entorhinal Cortex / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D004827:Epilepsy / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D007150:Immunohistochemistry; D007608:Kainic Acid / Q000494:pharmacology; D008297:Male; D019579:Neocortex / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D009498:Neurotoxins / Q000494:pharmacology; D009833:Olfactory Pathways / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D016760:Proto-Oncogene Proteins c-fos / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017470:Receptors, Glutamate / Q000187:drug effects / Q000378:metabolism*
D002135:Calcium-Binding Proteins; D018690:Excitatory Amino Acid Agonists; D009498:Neurotoxins; D016760:Proto-Oncogene Proteins c-fos; D017470:Receptors, Glutamate; D007608:Kainic Acid