Interaction of leptin and nitric oxide pathway on penicillin-induced epileptiform activity in rats

Aslan A., Yildirim M., Ayyildiz M., Guven A., Agar E.

BRAIN RESEARCH, vol.1321, pp.117-124, 2010 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 1321
  • Publication Date: 2010
  • Doi Number: 10.1016/j.brainres.2010.01.054
  • Journal Name: BRAIN RESEARCH
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.117-124
  • Karadeniz Technical University Affiliated: Yes


The aim of the present study was to investigate the role of NO as a mediator of leptin action at the penicillin-induced epileptiform activity in rat. Thirty minutes after penicillin injection, leptin, at a dose of 1 rig, significantly increased the mean frequency of epileptiform activity without changing the amplitude. The effects of systemic administration of nitric oxide synthase (NOS) inhibitors, non-selective NG-nitro-L-arginine methyl ester (L-NAME), selective neuronal NOS inhibitor, 7-nitroindazole (7-NI) and NO precursor, L-arginine on the effects of leptin were investigated. The occurrence of anticonvulsant activity of 7-NI (40 mg/kg, i.p.) was significantly delayed in the presence of leptin (1 mu g). The administration of L-NAME (60 mg/kg, i.p.), 30 mm before leptin (1 mu g) application, did not influence proconvulsant activity of leptin. The administration of L-arginine (1000 mg/kg, i.p.) 30 min before the effective dose of leptin (1 mu g, i.c.v.) reversed the proconvulsant effects of leptin whereas the same dose of its inactive enantiomer, D-arginine (1000 mg/kg, i.p.) failed to influence the proconvulsant effect of leptin. The electrophysiological evidence of the present study suggests that neuronal NOS/NO pathway is involved in mediating leptin effects on penicillin-induced epileptiform activity. (C) 2010 Elsevier B.V. All rights reserved.