SavedAdd your journal

Journals / Journal of Health Sciences and Medicine / 2023 / Cilt: 6 - Sayı: 1

Parallel changes in the promoter methylation of voltage-gated T-type calcium channel alpha 1 subunit G and histone deacetylase activity in the WAG/Rij model of absence epilepsy

Zülfinaz Betül ÇELİK
Emre Soner TİRYAKİ
Elif TÜRKDÖNMEZ
M. Nusret ÇİÇEKLİ
Ahmet ALTUN
Caner GÜNAYDIN
Pages
92–98
Publication Date
2023-01-12
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Results: Our results demonstrated that the number of SWDs increased age-dependent in WAG/Rij.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: In the last two decades, research on epigenetic mechanisms has expanded dramatically.
📊
Key Findings & Data:Recent studies demonstrated that epigenetic mechanisms regulate epilepsy and epileptogenic pathologies.
💡
Conclusion & Impact:Results: Our results demonstrated that the number of SWDs increased age-dependent in WAG/Rij.
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Epilepsy · voltage-gated T-type calcium channel · histone deacetylation

Abstract

Objective: In the last two decades, research on epigenetic mechanisms has expanded dramatically. Recent studies demonstrated that epigenetic mechanisms regulate epilepsy and epileptogenic pathologies. In this study, we aimed to investigate changes in the promoter methylation status of the voltage-gated T-type calcium channel alpha 1 subunit G (CACNA1G) gene and total histone deacetylase activity in Wistar Albino Glaxo/Rijswijk (WAG/Rij) rats which is one of the commonly used genetic absence rat models of epilepsy in the three different age groups (3, 6, and 9 months old) on both sexes. Material and Method: Evaluation of changes in the spike-wave discharges (SWDs) was performed with electrocorticography (ECoG). The promoter methylation status of the CACNA1G gene was determined by methylation-specific PCR (MSP), and histone deacetylase (HDAC) activity was determined spectrophotometrically. Results: Our results demonstrated that the number of SWDs increased age-dependent in WAG/Rij. Additionally, it was observed that CACNA1G promoter methylation decreased, and total HDAC activity increased with age in both sexes. Conclusion: Our results provide further support for epigenetic regulation in the absence epilepsy phenotype and suggest that the underlying mechanism behind the increase in the number of SWDs with age in the WAG/Rij animals might be regulated by CACNA1G promoter methylation or HDAC activity.

🔖

Cite This Article

ÇELİK, Z. B., TİRYAKİ, E. S., TÜRKDÖNMEZ, E., ÇİÇEKLİ, M. N., ALTUN, A., GÜNAYDIN, C. (2023). Parallel changes in the promoter methylation of voltage-gated T-type calcium channel alpha 1 subunit G and histone deacetylase activity in the WAG/Rij model of absence epilepsy. Journal of Health Sciences and Medicine, Cilt: 6 - Sayı: 1, 92–98. https://ajindex.com/articles/876382

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (8)

  1. van Luijtelaar G, van Oijen G. Establishing Drug Effects on Electrocorticographic Activity in a Genetic Absence Epilepsy Model: Advances and Pitfalls. Front. Pharmacol 2020; 11: 395. Ollivier ML, Dubois MF, Krajinovic M, Cossette P, Carmant L. Risk factors for valproic acid resistance in childhood absence epilepsy. Seizure 2009; 18: 690-4. Sarkisova K, van Luijtelaar G. The WAG/Rij strain: a genetic animal model of absence epilepsy with comorbidity of depression. Prog Neuropsychopharmacol Biol Psychiatry 2011; 35: 854-76. Coenen AML, van Luijtelaar ELJM. Genetic animal models for absence epilepsy: a review of the WAG/Rij strain of rats. Behav Genet 2003; 33: 635-55.
  2. Carney PW, Jackson GD. Insights into the mechanisms of absence seizure generation provided by EEG with functional MRI. Front Neurol 2014; 5: 162. Abderemane-Ali F, Findeisen F, Rossen ND, Minor Jr DL. A selectivity filter gate controls voltage-gated calcium channel calcium-dependent inactivation. Neuron 2019; 101: 1134-49.
  3. Weiss N, Zamponi GW. T-type calcium channels: from molecule to therapeutic opportunities. Int J Biochem Cell Biol 2019; 108: 34-9. Noebels JL. Calcium channel “gaiting” and absence epilepsy. Epilepsy Curr 2005; 5: 95-7.
  4. Glaba P, Latka M, Krause MJ, et al. Changes in interictal pretreatment and posttreatment EEG in childhood absence epilepsy. Front Neurosci 2020; 14: 196. Imbrici P. Dysfunction of the brain calcium channel CaV2.1 in absence epilepsy and episodic ataxia. Brain 2004;127: 2682-92.
  5. Ernst WL, Zhang Y, Yoo JW, Ernst SJ, Noebels JL. Genetic enhancement of thalamocortical network activity by elevating 1G-mediated low-voltage-activated calcium current induces pure absence epilepsy. J Neurosci 2009; 29: 1615-25.
  6. Lazarini-Lopes W, Campos-Rodriguez C, Palmer D, N’Gouemo P, Garcia-Cairasco N, Forcelli PA. Absence epilepsy in male and female WAG/Rij rats: a longitudinal EEG analysis of seizure expression. Epilepsy Res 2021; 176: 106693. Araki Y, Mimura T. The mechanisms underlying chronic inflammation in rheumatoid arthritis from the perspective of the epigenetic landscape. J Immunol Res 2016: 1-11.
  7. Araki Y, Mimura T. The histone modification code in the pathogenesis of autoimmune diseases. Mediators Inflamm 2017: 1-13.
  8. Percie du Sert N, Hurst V, Ahluwalia A, et al. The ARRIVE guidelines 2.0: Updated guidelines for reporting animal research. BMC Vet Res 2020; 16: 242. Doğan E, Aygün H, Arslan G, et al. The role of NMDA receptors in the effect of purinergic P2X7 receptor on