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Article
Author(s)

Betul Koklu1, Ayse Kristina Polat1, Ece Eroglu1, Irem Kullu1, Aslı Okan2, Zuleyha Doganyigit2 and Enes Akyuz3

Affiliation(s)

1. Faculty of Medicine, Yozgat Bozok University, Yozgat 66100, Turkey
2. Department of Histology and Embryology, Faculty of Medicine, Yozgat Bozok University, Yozgat 66100, Turkey
3. Department of Biophysics, Faculty of International Medicine, University of Health Sciences, Istanbul 34668, Turkey

ABSTRACT

Epilepsy is a disease with cardiovascular involvementdue to the disruptionof excitatory and inhibitory balance in the ANS (autonomic nervous system). Cardiac pathologies may occur as a result of dysfunction in vagus nerve. The vagus nerve, acetylcholine (ACh) secreted from efferent fibers interacts with α7 nicotinic ACh receptors (α7nAChR) on immune cells, preventing the release of cytokines such as HMGB1 and exerting a protective effect against inflammation. Kir6.2 channels are effective in the regulation of ACh release and inflammation in the vagus nerve to the heart in epilepsy. In addition to taking part in inflammation, HMGB1 regulates autophagy by interacting with Beclin 1, an essential molecule linked to autophagy.In our study, 35 mg/kg pentylenetetrazole (PTZ) agent was administered intraperitoneally to male and female rats and kindling model was created. We examined histologically the immunoreactivity of HMGB1, α7nAChR, Kir6.2 and Beclin 1 proteins in the heart and vagus nerve. Significant increases of HMGB1, α7nAChR, Kir6.2 and Beclin 1 immunoreactivity in the PTZ-kindled group compared to the control. With this study, a new perspective to understand may be provided in terms of inflammation, cardiac pathologies, and dysfunctions in epileptic seizures. It is important to carry out further studies to understand the relationship between the inflammation process and cardiac pathologies.

KEYWORDS

Inflammation, ACh, vagus nerve, heart, epilepsy.

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