Evaluation of the Role of Chronic Daily Melatonin Administration and Pinealectomy on Penicillin-Induced Focal Epileptiform Activity and Spectral Analysis of ECoG in Rats: An In Vivo Electrophysiological Study


Yildirim M., AYDIN-ABIDIN S., ABİDİN İ., Akca M., CANPOLAT S., CANSU A.

NEUROCHEMICAL RESEARCH, cilt.38, sa.8, ss.1672-1685, 2013 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 38 Sayı: 8
  • Basım Tarihi: 2013
  • Doi Numarası: 10.1007/s11064-013-1069-1
  • Dergi Adı: NEUROCHEMICAL RESEARCH
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.1672-1685
  • Karadeniz Teknik Üniversitesi Adresli: Evet

Özet

In the present study, we aimed to investigate the effects of pinealectomy and chronic melatonin administration on focal epileptiform activity induced by penicillin in the rat cortex and to determine the relation between melatonin levels and electrocorticogram (ECoG) power spectrum. For this purpose, male Sprague-Dawley rats were divided into six groups: control, sham operated, ethanol, melatonin, pinealectomy and pinealectomy + melatonin group. Melatonin-treated rats was intraperitoneally injected with a daily single dose of 10 mg/kg melatonin for 14 days, but the last dose was given 30 min after local application of penicillin as a convulsant agent. Focal epileptiform activity was produced by intracortical administration of penicillin (200 units/1 mu l). While chronic melatonin application did not affect either the onset latency or the spike frequency of epileptiform activity, pinealectomy significantly reduced latency to onset of initial epileptiform discharges and increased cortical epileptiform activity. However, acute melatonin administration decreased the epileptiform activity. The results also indicated that exogenously applied melatonin did not change the spectral analysis of ECoG, but pinealectomy led to a reduction in the power of the fast bands (gamma) power in ECoG. We conclude that endogenous melatonin signaling seem to have a tonic inhibitory action on neuronal excitability and epileptiform activity, and also a certain concentration of melatonin required for normal cortical excitability.