Contact us
 |
[email protected] |
 |
3275638434 |
 |
 |
| Paper Publishing WeChat |
Useful Links
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License
Article
Author(s)
Arda Kaan Üner1, Aslı Okan2, Enes Akyüz3 and Züleyha Doğanyiğit2
Full-Text PDF
XML 507 Views
DOI:10.17265/1548-6648/2022.01.002
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 34468, Turkey
ABSTRACT
Background: Epilepsy is a chronic neurological disease that occurs with recurrent seizures due to abnormal neuronal discharges in the brain. Glutamate has a role in the pathogenesis of epilepsy. Cardiac and respiratory system problems might be seen in epilepsy patients caused by autonomic dysfunction due to seizures. Hence, we aimed to investigate the expression of metabotropic glutamate receptor 5 (mGluR5) in the brainstem, vagus nerve, and heart tissues in an induced epilepsy model of rats. Materials and Methods: Pentylenetetrazole (PTZ) kindling model was induced in Wistar Albino rats. A total of 44 male and female rats were randomly divided into control and PTZ groups. Expression of mGluR5 in the heart, vagus nerve, and brainstem tissues was investigated by immunohistochemistry staining. Results: Obtained data showed that mGluR5 expression was significantly increased in female and male PTZ groups in vagus nerve and heart tissue. In the brainstem, mGluR5 expression was significantly increased in the male PTZ group compared to the control (p < 0.05). Significance: Our results show that mGluR5 expression is increased in heart, vagus nerve, and brainstem tissue in the epilepsy model induced with PTZ. These data demonstrate the possible role and significance of altered mGluR5 expression in epilepsy in autonomic dysfunction.
KEYWORDS
Epilepsy, autonomic dysfunction, SUDEP, seizure, glutamate.
Cite this paper
References