On the transcriptional level, TBB pretreatment led to differential gene expression changes of K Ca2.2, but also of HCN1 and HCN3 channels. Western blot analyses demonstrated that CA1 tissue from TBB-pretreated epileptic animals contained significantly less CK2 than TBB-pretreated controls. This was accompanied with a reduced proportion of burst firing neurons in the CA1 area. Results: We found that TBB pretreatment delayed onset of seizures after pilocarpine and slowed down disease progression during epileptogenesis. Methods: Here, we pretreated rats with TBB in vivo prior to the establishment of a pilocarpine-induced status epilepticus (SE) in order to analyze the long-term sequelae of such a preventive TBB administration. Previously, we observed that in vivo casein kinase 2 (CK2) inhibition with 4,5,6,7-tetrabromotriazole (TBB) had anti-epileptogenic effects in the acute epilepsy slice model. Purpose: Epilepsy therapy is currently based on anti-seizure drugs that do not modify the course of the disease, i.e., they are not anti-epileptogenic in nature. 4Center of Transdisciplinary Neurosciences Rostock, University of Rostock, Rostock, Germany.3German Center for Neurodegenerative Diseases (DZNE), Göttingen, Germany.2Department of Psychosomatic Medicine, Rostock University Medical Center, Rostock, Germany.
1Oscar Langendorff Institute of Physiology, University of Rostock, Rostock, Germany.Felix Schulze 1†, Steffen Müller 1†, Xiati Guli 1, Lukas Schumann 1, Hannes Brehme 1, Till Riffert 1, Marco Rohde 1, Doreen Goerss 2,3, Simone Rackow 1, Anne Einsle 1, Timo Kirschstein 1,4*† and Rüdiger Köhling 1,4*†
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