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Acta Physiologica Congress

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Acta Physiologica 2011; Volume 203, Supplement 686
Joint Congress of FEPS and Turkish Society of Physiological Sciences
9/3/2011-9/7/2011
Istanbul, Turkey


INDUCIBLE NITRIC OXIDE SYNTHASE ACTIVITY INVOLVES IN THE ANTICONVULSANT EFFECT OF GRAPE SEED EXTRACT ON PENICILLIN-INDUCED EPILEPTIFORM ACTIVITY IN RATS
Abstract number: PC095

Per1 Sedat, Tasdemir2 Abdulkadir, Yildirim3 Mehmet, Ayyildiz4 Mustafa, Ayyildiz2 Nusret, Agar4 Erdal

1Department of Biology, Bozok University, Yozgat, Turkey
2Department of Biology, Erciyes University, Kayseri, Turkey
3Department of Physiology, Karadeniz Technical University, Trabzon, Turkey
4Department of Physiology, Ondokuz Mays University, Samsun, Turkey

Objective: 

Grape seed extract (GSE) has been known to be neuroprotective due to its antioxidant properties. The aim of the present study was to examine both the effect of GSE on penicillin-induced epileptiform activity in rat and the role of the NO pathway in the effects of GSE.

Methods: 

In this study, sixty-six adult male Wistar rats weighing 225–260 g were used. The ECoG activity was continuously monitored on a four-channel recorder. All recordings were made under anesthesia and stored on a computer. The frequency and amplitude of epileptiform ECoG activity was analyzed offline.

Results: 

Intracortical injection of penicillin induced epileptiform activity. The best and earlier effects of selective inducible nitric oxide synthase inhibitor, aminoguanidin appeared at dose of 60 mg/kg, i.p. The effective dose of aminoguanidine (60 mg/kg, i.p.) partially reversed the anticonvulsant activity of GSE.The administration of the NO substrate, L-arginine (500 mg/kg, i.p.) 10 minutes before the effective dose of GSE (200 mg/kg, i.p.) blocked the influence of aminoguanidine on the anticonvulsant effect of GSE on penicillin-induced epileptiform activity. 7-NI significantly decreased the frequency of epileptiform ECoG activity without changing amplitude after 7-NI administration. However, the mean frequency of epileptiform activity was significantly decreased in the 50 min in the presence of L-arginine +GSE.

Conclusions: 

The anticonvulsant effect of GSE was diminished by the selective inducible NOS inhibitor, aminoguanidine, which was inhibited by L-arginine. Moreover, the nonspecific NOS inhibitor, L-NAME partially inhibited the anticonvulsant effect of GSE. Therefore, these findings imply that inducible-NOS participates in the anticonvulsant activity of GSE.

To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 203, Supplement 686 :PC095

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