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• W2020455511 abstract "Summary Objective The slow afterhyperpolarizing potential (s AHP ) following prolonged depolarization is a major intrinsic mechanism of neuronal inhibition, by powerfully dampening excitability for up to 2 s. Therefore, an altered sAHP function might be vulnerable to hyperexcitable states such as epilepsy. Here, we have investigated the role of casein kinase 2 ( CK 2) on the s AHP in control and chronically epileptic tissue. Methods Using the rat pilocarpine model of chronic temporal lobe epilepsy, we performed whole‐cell patch‐clamp recordings of acutely isolated CA 1 pyramidal cells and field potential measurements on hippocampal slices. Results Chronic oral administration of the CK 2 inhibitor 4,5,6,7‐tetrabromotriazole ( TBB ) for 4 days prior to brain dissection caused a significant increase of the s AHP ‐mediating current in both control and epileptic tissues. In contrast, when TBB was acutely applied during the patch‐clamp recording, the s AHP remained unaltered, indicating that chronic CK 2 inhibition was required for s AHP augmentation. To test whether CK 2 inhibition also has an anticonvulsive effect, we evoked recurrent epileptiform discharges ( RED s) in hippocampal slice preparations by M g 2+ removal. It is important to note that chronic oral TBB administration abolished RED s induced by 0‐ M g 2+ solution, suggesting that CK 2 inhibition indeed has anticonvulsive and perhaps antiepileptogenic properties. Significance Our data demonstrated that CK 2 inhibition augments the s AHP and might represent a novel mechanism of action of anticonvulsant drugs." @default.
• W2020455511 created "2016-06-24" @default.
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• W2020455511 date "2013-12-06" @default.
• W2020455511 modified "2023-10-04" @default.
• W2020455511 title "In vivo treatment with the casein kinase 2 inhibitor 4,5,6,7-tetrabromotriazole augments the slow afterhyperpolarizing potential and prevents acute epileptiform activity" @default.
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• W2020455511 doi "https://doi.org/10.1111/epi.12474" @default.
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