Calcium Channel Subunit α2δ4 Is Regulated by Early Growth Response 1 and Facilitates Epileptogenesis

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
Karen M J van LooS Schoch

Abstract

Transient brain insults, including status epilepticus (SE), can trigger a period of epileptogenesis during which functional and structural reorganization of neuronal networks occurs resulting in the onset of focal epileptic seizures. In recent years, mechanisms that regulate the dynamic transcription of individual genes during epileptogenesis and thereby contribute to the development of a hyperexcitable neuronal network have been elucidated. Our own results have shown early growth response 1 (Egr1) to transiently increase expression of the T-type voltage-dependent Ca2+ channel (VDCC) subunit CaV3.2, a key proepileptogenic protein. However, epileptogenesis involves complex and dynamic transcriptomic alterations; and so far, our understanding of the transcriptional control mechanism of gene regulatory networks that act in the same processes is limited. Here, we have analyzed whether Egr1 acts as a key transcriptional regulator for genes contributing to the development of hyperexcitability during epileptogenesis. We found Egr1 to drive the expression of the VDCC subunit α2δ4, which was augmented early and persistently after pilocarpine-induced SE. Furthermore, we show that increasing levels of α2δ4 in the CA1 region of the hippoca...Continue Reading

Citations

Mar 21, 2020·Annals of Neurology·Julika PitschAlbert J Becker
Jan 30, 2020·Frontiers in Cellular Neuroscience·Karen M J van Loo, Albert J Becker
Jul 2, 2020·Pflügers Archiv : European journal of physiology·Cornelia AblingerGerald J Obermair
Jan 7, 2021·Proceedings of the National Academy of Sciences of the United States of America·Miguel Rodríguez de Los SantosPeter M Krawitz
Sep 22, 2020·Cell Calcium·Dhanendra Tomar, John W Elrod
Jun 11, 2020·Current Opinion in Neurobiology·William Christopher Risher, Cagla Eroglu
Mar 31, 2021·Proceedings of the National Academy of Sciences of the United States of America·Clemens L SchöpfGerald J Obermair

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