Please use this identifier to cite or link to this item: http://hdl.handle.net/10201/22672

Title: Histone modifications in status epilepticus induced by Kainate
Issue Date: 2006
Publisher: Murcia : F. Hernández
ISSN: 0213-3911
Related subjects: CDU::6 - Ciencias aplicadas::61 - Medicina::615 - Farmacología. Terapéutica. Toxicología. Radiología
Keywords: Kainate
Status epilepticus
Abstract: Animal models of epilepsy have allowed the determination of the basic molecular and cellular mechanisms of epileptogenesis. Generalized limbic seizures and subsequent status epilepticus can be induced by either pilocarpine, the muscarinic acetylcholine receptor agonist or kainate, the glutamate receptor agonist. There has been increasing interest that chromatin remodeling might play a critical role in gene regulation even in non-dividing cells such as neurons. One form of chromatin remodeling is histone aminoterminal modification that can generate synergistic or antagonistic affinities for the interactions of transcriptional factors, in turn causing changes in gene activity. Two widely studied histone modification processes are histone acetylation and phosphorylation. While histone hyperacetylation indicates an increase in gene activity, its hypoacetylation marks gene repression. Both states are controlled by a dynamic interplay of histone acetyltransferase (HAT) and histone deacetylase (HDAC). We have found the upregulation of acetylation and phosphorylation of histones, coupled with status epilepticus after kainate administration. c-fos and c-jun mRNA have been sequentially induced in response to kainate, in different hippocampal subpopulations starting from the dentate gyrus and spreading to the cornus ammonis regions well correlated with the spatiotemporal distribution of histone H4 hyperacetylation. Both histone modifications are associated with the c-fos gene promoter after kainate stimulation, while only histone acetylation with the c-jun gene. Pretreatment with curcumin, which has a HAT inhibitory activity specific for CBP/p300, attenuates histone modifications, IEGs expression and also the severity of status epilepticus after kainate treatment. Histone modifications may have a crucial role in the development of epilepsy induced by kainate.
Primary author: Taniura, H.
Sng, J.C.G.
Yoneda, Y.
Published in: Histology and histopathology
URI: http://hdl.handle.net/10201/22672
Document type: info:eu-repo/semantics/article
Number of pages / Extensions: 7
Rights: info:eu-repo/semantics/openAccess
Appears in Collections:Vol.21, nº 7 (2006)

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