Involvement of nitric oxide pathway in the acute anticonvulsant effect of salmon calcitonin in rats

FİLİZ A. K., KARABULUT S.

EPILEPSY RESEARCH, cilt.180, 2022 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 180
  • Basım Tarihi: 2022
  • Doi Numarası: 10.1016/j.eplepsyres.2022.106864
  • Dergi Adı: EPILEPSY RESEARCH
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, PASCAL, Abstracts in Social Gerontology, BIOSIS, CAB Abstracts, EMBASE, MEDLINE, Veterinary Science Database
  • Anahtar Kelimeler: Salmon calcitonin, Pentylenetetrazole, Neuroinflammation, Nitric oxide, Rat, PENTYLENETETRAZOL-INDUCED SEIZURES, PTZ-INDUCED SEIZURES, BLOOD-FLOW CHANGES, KAINATE SEIZURES, SYNTHASE, BRAIN, HIPPOCAMPAL, INHIBITORS, EPILEPSY, MICE
  • Sivas Cumhuriyet Üniversitesi Adresli: Evet

Özet

Epilepsy is a chronic neurological disease that is thought to affect up to 1% of the world's population. Evidence suggests that salmon calcitonin (sCT) has positive effects on epileptic seizures and epileptogenesis. However, it remains unknown that whether nitric oxide (NO) pathway contributed to this antiepileptic effect of sCT. We have used the pentylenetetrazole (PTZ)-induced seizure rat model to identify the effect of sCT on seizure score, seizure-induced cognitive deficit, and the NO pathway in the brain. We found that sCT increases the first myoclonic jerk (FMJ), decreased Racine's convulsion scale (RCS), and abates seizure-induced cognitive impairment. We further demonstrated that sCT attenuated the abnormal increase of NO in the brain. These results revealed that sCT exerts an antiepileptic effect by modulating the NO pathway in the brain.