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Öğe Anticonvulsant effect of carnosine on penicillin-induced epileptiform activity in rats(Elsevier, 2008) Kozan, Ramazan; Sefil, Fatih; Bagirici, FarukCarnosine is a compound of naturally-occurring dipeptide that synthesized by the carnosine synthetase from beta-alanine and L-histidine. Recent reports claim that carnosine plays an important role in the control of epilepsy but its involvement in anticonvulsant functions remains unknown. In this study, we investigated the effects of carnosine in a rat model of epilepsy using the intracortical penicillin injection method. Thirty minutes after penicillin injection, the doses of 125, 250, 500, 1000 mg/kg carnosine and 90 min before penicillin injection the dose of 500 mg/kg carnosine were administered intraperitoneally. The epileptiform activity was verified by electrocorticographic (ECoG) recordings. The mean spike frequency of penicillin-induced epileptiform activity was significantly decreased in all carnosine-treated rats when compared with those of penicillin-injected. The dose of 500 mg/kg for carnosine treated and pretreated rats was found to be the most effective dose in reducing the frequency of penicillin-induced epileptiform activity. There was no significant difference in the mean onset of epileptiform activity between penicillin and 500 mg/kg camosine pretreated groups. These findings indicate that carnosine has an anticonvulsant effect on penicillin-induced epilepsy in rats. Thus, our data support the hypothesis that carnosine may be a potential anticonvulsant drug for clinical therapy of epilepsy in the future. (C) 2008 Elsevier B.V. All rights reserved.Öğe Bilateral high frequency stimulation of the subthalamic nucleus normalizes COX activity in the substantia nigra of Parkinsonian rats(Elsevier Science Bv, 2009) Vlamings, Rinske; Visser-Vandewalle, Veerle; Kozan, Ramazan; Kaplan, Suleyman; Steinbusch, Harry W. M.; Temel, YasinPart of the mechanism underlying the therapeutic effect of subthalamic nucleus (STN) high frequency stimulation (HFS) involves the activity of the basal ganglia output structures. The general idea is that STN's burst activity leads to an increased activity of the basal ganglia output nuclei and that HFS reverses this. However, the published data sets conflict. Here, we addressed the question which effect STN HFS had on the overall substantia nigra pars reticulata (SNr; one of the basal ganglia output nuclei) activity, in rats rendered Parkinsonian by 6-hydroxydopamine (6-OHDA) injections in the striatum, We used a marker for metabolic activity, cytochrome C oxidase (COX). The expression of COX in the SNr of Parkinsonian rats was significantly higher as compared to sham-operated rats. However, in Parkinsonian rats with STN HFS, expression of COX was significantly lower as compared to non-stimulated Parkinsonian rats, and was comparable to the level of expression in sham-operated rats. These results show that STN HFS decreased the overall activity of the basal ganglia output nucleus in dopamine-depleted rats. (C) 2009 Elsevier B.V. All rights reserved.Öğe Demirin neden olduğu purkinje hücre kaybı üzerine nitrik oksit sentaz inhibisyonunun koruyucu etkisi(2009) Sefil, Fatih; Kozan, Ramazan; Bostancı, Mehmet Ömer; Bağırıcı, FarukAmaç: Demir, nöronal hiperaktivite ve oksidatif stresi indüklemek için sıklıkla kullanılan bir metaldir. Nitrik oksit sentaz (NOS) tarafından sentezlenen nitrik oksit ile hücre ölümü arasındaki ilişkiyi ortaya koyan bulgular da mevcuttur. Bu çalışmada, intraserebroventriküler olarak injekte edilen demirin sıçan serebellar Purkinje hücrelerinde oluşturduğu nörotoksisiteye karşı bir indüklenebilir NOS inhibitörü olan aminoguanidin ve non-selektif NOS inhibötörü olan N-nitro-L- arjinin metil ester’in (L-NAME) etkisi araştırıldı. Gereç ve Yöntem: Sıçanlar; kontrol, demir, demir+aminoguanidin ve demir+L-NAME grupları olmak üzere dört gruba ayrıldı. Demir, demir+aminoguanidin ve demir+L-NAME gruplarındaki sıçanlara intraserebroventriküler olarak demir verildi. Operasyonu takiben on gün süreyle, demir+aminoguanidin ve demir+L-NAME gruplarındaki sıçanlara sırasıyla 30 mg/kg aminoguanidin ve 60 mg/kg L-NAME intraperitoneal olarak verildi. Onuncu günün sonunda, bütün gruplardaki hayvanlar üretan anestezi altında intrakardiyak yolla perfüze edildi. Toplam Purkinje hücre sayımları için tarafsız sayım metodu olan stereolojik yöntem kullanıldı. Bulgular: Demir+aminoguanidin ve demir+L- NAME grupları demir grubu ile karşılaştırıldığında, aminoguanidin ve L-NAME demirin indüklediği Purkinje hücre kaybını %24.9’dan sırasıyla %12.3 ve %11.3’e gerilettiği bulundu (p<0.05). Sonuç: Bu çalışmanın sonuçları, aminoguanidin ve L-NAME’nin demirin indüklediği Purkinje hücre kaybını anlamlı olarak azalttığını ve NOS inhibisyonunun demirin zararlı etkilerini önleyebileceğini gösterdi.Öğe Inhibition of neuronal nitric oxide synthase prevents iron-induced cerebellar Purkinje cell loss in the rat(Nencki Inst Experimental Biology, 2008) Gulturk, Sefa; Kozan, Ramazan; Bostanci, M. Omer; Sefil, Fatih; Bagirici, FarukIron plays an important role in maintaining normal. brain function. However, in many neurodegenerative diseases abnormal iron accumulation in specific brain regions has been consistently reported. In this study, we investigated the neurotoxic effect of the intracerebroventricularly injected iron on the cerebellar Purkinje cells in the rat and the role of nitric oxide (NO) in this process. The role of NO in rats administered iron (FeCl(3)6H(2)O) was examined with the use of a donor of NO, L-arginine (L-Arg), and a central selective inhibitor of NO synthase, 7-nitroindazole (7-NI). For this reason, rats were divided into 5 groups: control, iron-injected, iron plus L-Arg, iron plus 7-NI, and iron plus L-Arg plus 7-NI. Means (value standard deviation) of the total numbers of Purkinje cells in the cerebellum were estimated as 337 +/- 23, 209 +/- 16, 167 +/- 19, 305 26, and 265 +/- 14 thousands in the control, iron, iron plus L-Arg, iron plus 7-NI, and iron plus L-Arg plus 7-NI groups, respectively. Iron treatment alone and the combination of iron and L-Arg caused a significant reduction in the total number of cerebellar Purkinje cells. Therefore, L-Arg increased the Purkinje cell loss induced by treatment with iron. These data show that inhibition of the neuronal NOS by 7-NI can prevent some of the deleterious effects of iron on cerebellar Purkinje cells. Presence of L-arginine decreased the neuroprotective effect of 7-NI.Öğe Interaction between carbenoxolone and valproic acid on pentylenetetrazole kindling model of epilepsy(E-Century Publishing Corp, 2015) Sefil, Fatih; Arik, Aliye E.; Acar, Meryem D.; Bostanci, Mehmet O.; Bagirici, Faruk; Kozan, RamazanGap junctions play an important role in the synchronized neuronal discharges. The main reason of the epileptic seizures is disruption of this synchronization. Therefore, the aim of the present study is to explore the combination valproic acid with carbenoxolone in pentylenetetrazole-kindled rats. In the first set of experiments, pentylenetetrazole (35 mg/kg intraperitoneally was administered to the rats to produce the kindling and then permanent screw electrodes to record electroencephalographic signals. The kindled rats were divided into six groups. While electroencephalographic recordings received from animals, behavioral evaluation was done by an observer. The data analysis was performed using T test and Mann-Whitney U tests. The dose of 40 mg/kg carbenoxolone was the most effective in carbenoxolone treatment groups. It prevented generalized seizures by 50%, reduced seizure stage, seizure duration and spike frequency. There was no significant difference between carbenoxolone-valproic acid combination and valproic acid on any seizure parameters. The current study is the first study which shows the interaction of carbenoxolone with valproic acid in pentylenetetrazole kindling model. As a result, carbenoxolone-valproic acid combination was not more effective than the standalone use of these drugs.Öğe Iron-Induced Cerebellar Purkinje Cell Loss Is Ameliorated by Flunarizine(Tubitak Scientific & Technological Research Council Turkey, 2009) Kozan, Ramazan; Bostanci, M. Oemer; Nacar, Tuncer; Aslan, Ali; Bagirici, FarukAim: In this study, we investigated the effect of intracerebroventricular-injected iron neurotoxicity on the total number of cerebellar Purkiinje cells in rats and the possible neuroprotective effect of flunarizine, a piperazine-derived calcium channel blocker. Materials and Methods: Rats were divided into four groups: control, flunarizine. iron, and iron + flunarizine groups. Rats in the iron and iron + flunarizine groups received intracerebro-ventricular iron (FeCl36H2O. 200 mM, 2.5 mu l), while those in flunarizine and iron + flunarizine groups were intraperitoneally injected with flunarizine (10 mg/kg/day) once a day after the operation for 10 days. After 10 days, all rats were perfused intracardially and then sacrificed. Brain tissues were removed and standard histological techniques were performed. The total numbers of Purkinje cells were estimated using unbiased stereological techniques. Results: Means of the total numbers of Purkinje cells in the cerebellum were estimated as 310441 +/- 6558, 298658 +/- 9636, 200201 +/- 6822 and 282658 +/- 6327 in the control, flunarizine, iron, and iron + flunarizine groups. respectively. Comparison between iron and iron + flunarizine groups revealed that flunarizine significantly attenuates the iron-induced neuron loss from 35.5% to 8.9% (P < 0.05). Conclusions: Findings of the present study suggest that flunarizine has a neuroprotective effect on iron-induced Purkinje cell loss in the rat cerebellum via blocking influx of calcium ions into neurons.Öğe Iron-induced cerebellar purkinje cell loss is ameliorated by flunarizine(2009) Kozan, Ramazan; Bostancı, Mehmet Ömer; Nacar, Tuncer; Aslan, Ali; Bağırıcı, FarukAim: In this study, we investigated the effect of intracerebroventricular-injected iron neurotoxicity on the total number of cerebellar Purkinje cells in rats and the possible neuroprotective effect of flunarizine, a piperazinederived calcium channel blocker. Materials and Methods: Rats were divided into four groups: control, flunarizine, iron, and iron + flunarizine groups. Rats in the iron and iron + flunarizine groups received intracerebro-ventricular iron (FeCl36H2O, 200 mM, 2.5 μl), while those in flunarizine and iron + flunarizine groups were intraperitoneally injected with flunarizine (10 mg/kg/day) once a day after the operation for 10 days. After 10 days, all rats were perfused intracardially and then sacrificed. Brain tissues were removed and standard histological techniques were performed. The total numbers of Purkinje cells were estimated using unbiased stereological techniques. Results: Means of the total numbers of Purkinje cells in the cerebellum were estimated as 310441 ± 6558, 298658 ± 9636, 200201 ± 6822 and 282658 ± 6327 in the control, flunarizine, iron, and iron + flunarizine groups, respectively. Comparison between iron and iron + flunarizine groups revealed that flunarizine significantly attenuates the iron-induced neuron loss from 35.5% to 8.9% (P < 0.05). Conclusions: Findings of the present study suggest that flunarizine has a neuroprotective effect on ironinduced Purkinje cell loss in the rat cerebellum via blocking influx of calcium ions into neurons.Öğe Nitric oxide, lipid peroxidation, and antioxidant enzyme levels in epileptic children using valproic acid(Elsevier Science Bv, 2009) Peker, Erdal; Oktar, Sueleyman; An, Mustafa; Kozan, Ramazan; Dogan, Murat; Cagan, Eren; Soeguet, SadikIn the present study, we investigated the effects of valproic acid (VPA) on nitric oxide (NO) level, lipid peroxidation, and antioxidant enzyme activities in 21 epileptic children and 26 healthy controls. The subjects were selected from those who visited for a checkup or medical treatment at the Mustafa Kemal University Research Hospital. Serum levels of NO-2, NO-3, malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) were analyzed by redox or enzymatic reactions and spectrophotometry. Based on the NO-2 and NO-3 levels, the NO concentration was about 10% higher in VPA group than in the control group (p < 0.001). However, no significant difference was detected for serum MDA, SOD, and CAT levels. It is suggested that NO would play a role in the mechanism of antiepileptic effects by VPA treatment. (c) 2009 Elsevier B.V. All rights reserved.Öğe Sıçan serebellumunda demir nörotoksisitesine karşı vitamin E'nin koruyucu etkisi(2009) Kozan, Ramazan; Bostancı, Mehmet Ömer; Ayas, Bülent; Aslan, Ali; Bağırıcı, FarukAmaç: Bu çalışmada, intraserebroventriküler olarak verilen demirin, sıçan serebellar Purkinje hücrelerinde oluşturduğu nörotoksisiteye karşı yağda çözülebilen güçlü bir antioksidan olan vitamin E'nin (?-tokoferol) etkisini araştırdık. Gereç ve Yöntem: Sıçanlar, kontrol, demir ve demir+vitamin E grupları olmak üzere üç gruba ayrıldı. Demir ve demir+vitamin E gruplarındaki sıçanlara intraserebroventriküler olarak demir (FeCl36H2O, 200 mM, 2.5 ?l) verildi. Demir+vitamin E grubundaki sıçanlara operasyonu takiben on gün süreyle 100 mg/kg/gün dozunda vitamin E intraperitoneal olarak verildi. Onuncu günün sonunda, bütün gruplardaki hayvanlar intrakardiyak yolla perfüze edildikten sonra dekapite edildiler. Beyin dokuları çıkarılarak standart histolojik doku takibi uygulandı. Toplam Purkinje hücre sayıları tarafsız sayım metodu olan stereolojik yöntemle hesaplandı. Bulgular: Ortalama toplam Purkinje hücre sayıları, kontrol grubunda 490584±13286; demir grubunda 331497±10764 ve demir+vitamin E grubunda 412118±15842 olarak bulundu. Demir ve demir+vitamin E grupları karşılaştırıldığında, vitamin E'nin demirin indüklediği Purkinje hücre kaybını %32.4'den %15.9'a düşürdüğü bulundu (p<0.01). Sonuç: Bu çalışmanın sonuçları, vitamin E'nin sıçan serebellumunda demirin indüklediği Purkinje hücre kaybını dikkate değer ölçüde geri çevirdiğini gösterdi. Bu nöroprotektif etkinin, vitamin E'nin serbest radikaller üzerine antioksidan aktivitesinden kaynaklandığı düşünülmektedir.
