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The Effect of Post-Learning REM Sleep Deprivation on Hipocampal REST Tomosyn Expression in Mice
(WILEY, 2017) Karabulut, Sebahattin; Bayramov, Kezban Korkmaz; Ozdemir, Fadime; Topaloglu, Tugba; Ergen, Ergul; Taskiran, Ahmet Sevki; Golgeli, Asuman
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Effect of the allopregnanolone and allotetrahydrodeoxycorticosteron on spike-wave discharges in the EEG of absence epilepsy rat models
(GENERAL PHYSIOL AND BIOPHYSICS, 2018) Karabulut, Sebahattin; Bayramov, Ruslan; Bayramov, Keziban Korkmaz; Filiz, Ahmet K.; Taskiran, Ahmet S.; Ozdemir, Ercan
Absence epilepsy is a generalized nonconvulsive type of epilepsy that is characterized by spike-wave discharges (SWD) with a frequency of 2.5-4 Hz in the EEG. The activation of the GABAergic system in central nervous system suppresses convulsive seizures but exacerbates absence seizures. Endogenous neuroactive steroids such as 3 alpha-hydroxy-5 alpha-pregnan-20-one (3 alpha,5 alpha-THPROG; allopregnanolone) and 3 alpha,21-dihydroxy-5 alpha-pregnan-20-one (3 alpha,5 alpha-THDOC, allotetrahydrodeoxycorticosteron) are GABA-A receptor-positive allosteric modulators. Finasteride which is a 5 alpha-reductase inhibitor can selectively block the synthesis of endogenous steroids. In this study, we compared the effects of endogenous steroids (THPROG and THDOC) on SWD by using finasteride-treated Wistar Albino Glaxo from Rijswijk (WAG/Rij) rats as a model of absence epilepsy. Wistar (WIS-THPROG and WIS-THDOC) and WAG/Rij (WAG-THPROG and WAG-THDOC) rats were divided into 4 groups (n = 8). After stereotactic surgical procedures, all rats were prepared for direct cortical EEG measurement. Following finasteride administration to each group, THPROG was administered to WIS-THPROG and WAG-THPROG groups, and THDOC to WIS-THDOC and WAG-THDOC groups intraperitoneally. While there was no any SWD activity detected in WIS-THPROG and WIS-THDOC groups, a significant increase in SWD count in WAG-THPROG = 0.012) and in WAG-THDOC (p = 0.012), and in SWD total duration in WAG-THPROG (p = 0.012) and WAG-THDOC groups (p = 0.011) were observed after steroid injection. No difference between the efficacy of THPROG and THDOC on absence seizures in WAG/Rij rats was observed.
Effects of post-learning REM sleep deprivation on hippocampal plasticity-related genes and microRNA in mice
(ELSEVIER SCIENCE BV, 2019) Karabulut, Sebahattin; Bayramov, Keziban Korkmaz; Bayramov, Ruslan; Ozdemir, Fadime; Topaloglu, Tugba; Ergen, Ergul; Yazgan, Kamile; Taskiran, Ahmet Sevki; Golgeli, Asuman
Sleep is essential for memory consolidation that stabilizes a memory trace. Memory consolidation includes waves of new gene expression and protein synthesis. Recently, microRNAs (miRNAs) have emerged as critical regulators of memory processes. Previous studies demonstrated that rapid eye movement (REM) sleep deprivation (REM SD) during specific time windows after training in the Morris water maze (MWM) task impairs memory consolidation. Here, we showed that the post-learning REM sleep, extending from 3 to 6 h after last training, is critical for spatial learning in the MWM task. Further, we found that the REM SD after training significantly changes the hippocampal expression of brain-derived neurotrophic factor (BDNF) mRNA; however, it causes minimal difference in the hippocampal expressions of calcium-calmodulin-dependent protein kinase II (CAMKII) and cAMP response-element-binding (CREB). In addition, it considerably affected the hippocampal expressions of miR-132, miR-182, and miR-124. In conclusion, after the MWM task, the post-learning REM sleep during specific time windows can modulate spatial memory consolidation, and its deprivation can impact the hippocampal transcriptional processes including memory-related miRNAs and mRNAs.
Evaluation of TRPM2 Channel-Mediated Autophagic Signaling Pathway in Hippocampus and Cortex Tissues of Rat Offspring Following Prenatal Exposure to Elevated Alcohol Levels
(John Wiley and Sons Inc, 2024) Uğuz, Abdülhadi Cihangir; Okan, Aslı; Doğanyiğit, Züleyha; Yilmaz, Seher; Ateş, Şükrü; Arikan Söylemez, Evrim Suna; Karabulut, Sebahattin
Fetal alcohol syndrome (FAS) can occur because of high amount of alcohol intake during pregnancy and is characterized by both physical and neurological problems. Children diagnosed with FAS have difficulties in learning, memory, and coordination. Hippocampus has a major role in memory and learning. We aimed to determine whether alcohol exposure during pregnancy had any effect on offspring by evaluating learning ability as well as oxidative stress and autophagy in the hippocampus and cortex tissues of litters. Attention was also paid to sex differences. To do so, TRPM2, Beclin1, p62, LC3B, IBA1, parvalbumin, GAD65, and mGluR5 expression levels were evaluated by immunohistochemistry. Lactate dehydrogenase (LDH), and malondialdehyde (MDA) levels, as well as total oxidant (TOS) and total antioxidant (TAS) status were determined by ELISA. Learning experiments were evaluated by the Morris water maze (MWM) test. Our findings demonstrated that IBA1, LC3B, GAD65, and mGluR5 expression levels were higher in female rats of the chronic alcohol exposure (CAE) model. Our IHC results revealed that TRPM2 expression levels were significantly increased in both males and females in the CAE group. Likewise, TAS was lower, and TOS was higher in CAE animals. Moreover, MWM outcomes supported a learning deficiency in CAE litters compared to controls and indicated that female offspring outperformed males in learning experiments. Therefore, our results revealed the detrimental effects of alcohol exposure during pregnancy on autophagy signaling in the hippocampus and cortex tissue of litters, which could affect the learning ability of animals. © 2024 The Author(s). Environmental Toxicology published by Wiley Periodicals LLC.
Farelerde Pentilentetrazol ile Oluşturulan Epileptik Nöbetler Üzerine Anakinra’nın Etkisinin Araştırılması
(2021) Filiz, Ahmet Kemal; Karabulut, Sebahattin
Amaç: Beyinde gama aminobutirik asit (GABA) ve glutamat arasındaki dengenin bozulması, nöbet oluşumuna ve epileptogenezekatkı sağlayan önemli faktörlerden biridir. Bu çalışmanın amacı, anakinra ön tedavisinin pentilentetrazol (PTZ) ile oluşturulan nöbetmodelinde kortikal ve hipokampal GABA ve glutamat seviyeleri üzerine etkisinin olup olmadığını belirlemektir.Araçlar ve Yöntem: Çalışmada 18 adet BALB-c türü fare Kontrol, PTZ ve Anakinra grupları şeklinde 3 gruba ayrıldı. Nöbetleribaşlatmak için 60 mg/kg dozda PTZ enjeksiyonu farelere intraperitonal olarak uygulandı. Anakinra grubuna PTZ enjeksiyonundan 30dakika önce intraperitonal olarak anakinra (100 mg/kg) uygulandı. Hayvanların kortikal ve hipokampal GABA ve glutamat düzeyleriEnzyme Linked Immunosorbent Assay (ELISA) yöntemi kullanılarak ölçüldü.Bulgular: PTZ'nin neden olduğu nöbetler, hipokampusta glutamat seviyesini artırırken (p<0.001), GABA düzeyinde azalmaya yolaçtı (p<0.05). PTZ tedavisi kortikal glutamat seviyesini arttırdı (p<0.05). Anakinra ile ön tedavi hipokampusta glutamat düzeyiniazaltırken (p<0.001), GABA düzeyinde artışa yol açtı (p<0.01). Ayrıca anakinra ön tedavisi kortikal glutamat seviyesini azaltırken(p<0.05), GABA düzeyinde artışla sonuçlandı (p<0.001).Sonuç: PTZ'nin neden olduğu nöbetler beyinde GABA düzeyinin azalmasına ve glutamat seviyesinin artışına neden olmaktadır. PTZenjeksiyonu öncesinde anakinra tedavisi farelerin beyinlerinde uyarılma lehine bozulmuş GABA/Glutamat dengesizliğini iyileştirmektedir
Farelerde Pentilentetrazol ile Oluşturulan Epileptik Nöbetler Üzerine Anakinra’nın Etkisinin Araştırılması
(Kırşehir Ahi Evran Üniversitesi, 2021) Filiz, Ahmet Kemal; Karabulut, Sebahattin
Amaç: Beyinde gama aminobutirik asit (GABA) ve glutamat arasındaki dengenin bozulması, nöbet oluşumuna ve epileptogeneze katkı sağlayan önemli faktörlerden biridir. Bu çalışmanın amacı, anakinra ön tedavisinin pentilentetrazol (PTZ) ile oluşturulan nöbet modelinde kortikal ve hipokampal GABA ve glutamat seviyeleri üzerine etkisinin olup olmadığını belirlemektir.Araçlar ve Yöntem: Çalışmada 18 adet BALB-c türü fare Kontrol, PTZ ve Anakinra grupları şeklinde 3 gruba ayrıldı. Nöbetleri başlatmak için 60 mg/kg dozda PTZ enjeksiyonu farelere intraperitonal olarak uygulandı. Anakinra grubuna PTZ enjeksiyonundan 30 dakika önce intraperitonal olarak anakinra (100 mg/kg) uygulandı. Hayvanların kortikal ve hipokampal GABA ve glutamat düzeyleri Enzyme Linked Immunosorbent Assay (ELISA) yöntemi kullanılarak ölçüldü.Bulgular: PTZ'nin neden olduğu nöbetler, hipokampusta glutamat seviyesini artırırken (p<0.001), GABA düzeyinde azalmaya yol açtı (p<0.05). PTZ tedavisi kortikal glutamat seviyesini arttırdı (p<0.05). Anakinra ile ön tedavi hipokampusta glutamat düzeyini azaltırken (p<0.001), GABA düzeyinde artışa yol açtı (p<0.01). Ayrıca anakinra ön tedavisi kortikal glutamat seviyesini azaltırken (p<0.05), GABA düzeyinde artışla sonuçlandı (p<0.001).Sonuç: PTZ'nin neden olduğu nöbetler beyinde GABA düzeyinin azalmasına ve glutamat seviyesinin artışına neden olmaktadır. PTZ enjeksiyonu öncesinde anakinra tedavisi farelerin beyinlerinde uyarılma lehine bozulmuş GABA/Glutamat dengesizliğini iyileştir-mektedir.
FGF-18'in SH-SY5Y Hücre Hattında Glutamat Eksitotoksisitesi Üzerine Etkisi
(Sivas Cumhuriyet Üniversitesi, 2023) Yıldız, Talha; Karabulut, Sebahattin; Bolat, Melike; Yalçınkaya, Melike
Bu çalışmada, aşırı glutamatın neden olduğu hücresel hasara karşı FGF-18'in olası nöroprotektif etkisini ve oksidan-antioksidan dengesindeki iyileşmenin bu etkide rol oynayıp oynamadığını araştırdık. Beyindeki nöronların yaklaşık %90'ı tarafından kullanılan ana uyarıcı nörotransmitter olan glutamat, öğrenme, hafıza ve biliş gibi çok sayıda nöronal sürecin normal işleyişi için kritik öneme sahiptir. İnsan beyninde 6-7 μmol/g glutamat, glutamin ile birlikte merkezi sinir sisteminde en bol bulunan serbest amino asittir. Glutamat eksitotoksisitesi, aşırı glutamatın sinir hücrelerine verdiği zarar olarak tanımlanır ve iyonotropik glutamat reseptörlerinin (iGluR) anormal aktivasyonundan kaynaklanır. Eksitotoksisite nöronal hücre ölümüne yol açabilir. Fibroblast büyüme faktörleri (FGF'ler) hücre çoğalması, hayatta kalma ve göç dahil olmak üzere birçok hücresel işlevden sorumlu sinyal molekülleridir. FGF-18, insanlarda FGF-18 geni tarafından kodlanan bir büyüme faktörüdür. Bu çalışmada, glutamat eksitotoksisitesinin birçok nörodejeneratif hastalığın fizyopatolojisinde yer aldığını göz önünde bulundurarak, FGF-18'in olası nöroprotektif etkisini ve bu etkide oksidatif stresin rolünü araştırdık. Deneyde, glutamat eksitotoksisitesine maruz bırakılan SH-SY5Y hücre hattında FGF-18 tedavisinin hücre sağkalımı üzerindeki etkisi XTT yöntemi ile değerlendirilmiştir. Ayrıca, FGF-18'in oksidatif stres üzerindeki etkisini değerlendirmek için ELISA yöntemi ile total antioksidan (TAS) ve total oksidan (TOS) seviyeleri ölçülmüştür. Sonuçlar, FGF-18'in glutamat eksitotoksisitesi üzerinde doğrudan bir etkisi olmamasına rağmen, sağkalımı artırdığını ve oksidatif stres üzerinde olumlu bir etkisi olduğunu göstermiştir.
Finasterid uygulanan absans epileptik sıçanlarda nöroaktif steroidler olan allotetrahidrodeoksikortikosteron ve allopregnanolon’ un EEG’ de diken dalga deşarjlara etkisi
(Cumhuriyet Üniversitesi, 2013) Karabulut, Sebahattin; Gültürk, Sefa
Absans epilepsi jeneralize epilepsinin non-konvülsif bir formu olup, EEG? de 2,5-4 Hz frekansındaki diken ve yavaş dalga deşarj (DDD) aktivitesiyle karakterizedir. Merkezi sinir sisteminde GABAerjik sistemin aktivasyonu konvülsif tarzdaki nöbetleri baskılarken, absans nöbetleri şiddetlendirir. Endojen nöroaktif steroidler olan pregnanolon metabolitleri 3?-hidroksi-5?-pregnan-20-one (3?,5?-THPROG; Allopregnanolon) ve 3?,21-dihidroksi-5?- pregnan-20-one (3?,5?-THDOC; Allottetrahidrodeoksikortikosteron) GABA-A reseptörlerinin en güçlü pozitif allosterik modülatörleri olup, hem fizyolojik hem de patolojik koşullarda GABAerjik sistemi etkileyebilirler. Bir 5?-redüktaz inhibitörü olan finasterid endojen steroidlerin sentezini seçici olarak bloke edebilir. Bu çalışmada, finasterid uygulanmış absans epilepsinin genetik bir modeli olan WAG/Rij sıçanlarda DDD? lere endojen steroidler olan THPROG ve THDOC?un etkilerinin karşılaştırılması amaçlanmıştır. Wistar (Grup 1 ve Grup 2) ve WAG/Rij (Grup 3 ve Grup 4) sıçanlardan 4 grup oluşturuldu (n=8). Stereotaksik cerrahi işlemlerden sonra tüm sıçanlar direkt kortikal EEG ölçümüne hazır hale getirildiler. Her gruba finasterid uygulandıktan sonra Grup 1 ve 3? e THPROG, Grup 2 ve 4?e THDOC ip yolla verildi. Grup 1 ve 2? de herhangi bir DDD aktivitesi gözlenmezken, Grup 3 ve 4? de steroid enjeksiyonundan sonra DDD sayısında (p=0,012) ve DDD toplam süresinde (sırasıyla p=0,012; p=0,011) bir artış görülmüştür. Ayrıca Grup 3? de ortalama DDD süresindeki artış Grup 4? e kıyasla daha fazla olmuştur (p=0,007). Sonuç olarak, THPROG WAG/Rij sıçanlarda absans nöbetlerde daha fazla artışa neden olmuştur. Bazal koşullar altında absans nöbetlerin regülasyonunda THPROG daha ön planda görülmektedir.
GSK461364A suppresses proliferation of gastric cancer cells and induces apoptosis
(Pergamon-Elsevier Science Ltd, 2023) Ataseven, Dilara; Tastemur, Seyma; Yulak, Fatih; Karabulut, Sebahattin; Ergul, Mustafa
Polo-like kinase 1 (PLK1) is crucial in regulating cell division and has been shown to have an oncogenic function in several cancers. Since PLK1 overexpression is closely related to tumorigenesis and has been correlated with poor clinical outcomes, specific inhibition of PLK1 in cancer cells is a promising approach for developing new anticancer drugs. In this context, the aim of the present study was to evaluated the potential cytotoxic effects of GSK461364A, a competitive inhibitor for PLK1, in gastric cancer cell line SNU-1 cells and explored its cytotoxic mechanism. The cells were exposed to GSK461364A at different concentrations ranging from 1 to 40 mu M for 24 h, and it showed considerable cytotoxicity with an IC50 value of 4.34 mu M. The treatment of SNU-1 cells with GSK461364A results in cell cycle arrest at the G2/M phase, decreased mitochondrial membrane potential, and increased apoptosis as indicated by Annexin V binding assay. In addition, GSK461364A treatment significantly increased the total oxidant (TOS) level, a signal of oxidative stress, and increased cleaved PARP and 8-oxo-dG levels as an indicator of DNA damage. ELISA experiments evaluating Bax, BCL-2, and cleaved caspase 3 also confirmed the apoptotic effect of GSK461364A. Current findings suggest that GSK461364A may be a chemotherapeutic agent in patients with gastric cancer. Nevertheless, more research is needed to evaluate GSK461364A as a cancer treatment drug.
Investigation of the effect of REM sleep deprivation on epileptic seizures caused by pentylenetetrazole in mice
(2020) Akkaya, Recep; Karabulut, Sebahattin; Taşkıran, Ahmet Şevki
Aim: To investigate whether different periods of rapid eye movement sleep deprivation (REM SD)contribute to seizure susceptibility, hippocampal oxidative status and balance of inhibition-excitationin the acute epilepsy model.Methods: REM SD was performed using the modified multiple platforms method on adult maleBALB/c mice. Pentylentetrazol (PTZ) was injected to induce seizures and hippocampal totalantioxidant status (TAS), total oxidant status (TOS), gamma aminobutyric acid (GABA), andglutamate levels were measured using the ELISA method.Results: PTZ-induced seizures following 8 h and 72 h REM SD significantly reduced thehippocampal TAS levels, but did not affect the TOS levels. In REM SD groups, especially after 8hours of REM sleep loss, there was a significant increase in glutamate in PTZ induction. Thehippocampal GABA levels were increased by PTZ-induced seizures after 72 h REM SD. PTZinduction after 8 hours of RAM SD leads to a significant increase in the seizure duration.Conclusion: It can be speculated that the REM SD can contribute to seizure susceptibility bychanging the oxidant-antioxidant balance and excitatory and inhibitory tone in the hippocampus.
Involvement of nitric oxide pathway in the acute anticonvulsant effect of salmon calcitonin in rats
(Elsevier, 2022) Filiz, Ahmet Kemal; Karabulut, Sebahattin
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.
Meloxicam, a selective COX-2 inhibitor, displays anticonvulsive effects in pentylenetetrazoleinducedacute seizures in mice through GABA and glutamate mediated mechanism
(2022) Sahın, Bilal; Akkaya, Recep; Karabulut, Sebahattin
Aim: To investigate the possible anticonvulsive effect of the selective COX-2 inhibitor meloxicam in\rpentylenetetrazole (PTZ)-induced epileptic seizures in mice and to examine its possible role on inhibition and\rexcitation balance in the brain.\rMethod: 30 BALB-c albino mice (16-18 weeks old) weighing 30-33 gr were used. Animals were randomly\rdivided into five groups (n = 6 for each group). Group 1: control, group 2: received saline (10 ml/kg, i.p.) 30\rminutes before PTZ (60 mg/kg i.p.) administration, group 3: received saline (10 ml/kg, i.p.) 30 minutes after\rPTZ (60 mg/kg i.p.) injection, group 4: received 60 mg/kg meloxicam i.p., 30 minutes before PTZ (60 mg/kg\ri.p.) administration. Group 5: received meloxicam (60 mg/kg i.p.) 30 minutes after PTZ injection (60 mg/kg,\ri.p.). The animals were observed for 30 minutes and the seizure stages and first myoclonic jerk times (FMJ)\rwere recorded. After 24 hours, brain tissues were removed and the cortex and hippocampus were separated for\rbiochemical assessments. ELISA method was used to measure GABA and glutamate levels.\rResults: Administration of meloxicam before PTZ induced seizure, reduced seizure stages and prolonged FMJ\rduration (p<0.05). Pre-treatment with meloxicam increased GABA levels in the cortex and decreased\rglutamate levels in the hippocampus (p<0.05). Post-treatment of meloxicam after PTZ-induced seizure\rincreased GABA levels in the hippocampus (p<0.05).\rConclusion: The results of our experimental study suggest that meloxicam has anti-convulsive effects and\rthese effects may be mediated by GABA and glutamate, which are the main indicators of inhibition and\rexcitation balance in the brain.
Neuroprotective effect of astaxanthin (ATX) against cognitive impairment on PTZ-induced epileptic seizures in rats and against PTZ-induced neurotoxicity in SH-SY5Y human neuroblastoma cell culture
(Sivas Cumhuriyet University, 2019) Karademir, Mustafa; Gümüş, Erkan; Taştemur, Yaşar; Ergül, Merve; Ergül, Mustafa; Karabulut, Sebahattin; Akkaya, Recep
Objective: Epilepsy is a common brain disorder that seizures could cause neuronal loss in the hippocampus. Oxidative stress has an important role in the pathology of this way. The aim of this study was to investigate the neuroprotective effect of astaxanthin (ATX), on pentylenetetrazole (PTZ) induced epileptic seizures in rats and in SH-SY5Y human neuroblastoma cell culture.Method: In our study, we used 42 male 230-250 g Wistar Albino rats. Animals were divided into seven groups as control, saline (PTZ; 1 ml/kg serum physiologic), positive control (2,5 mg/kg diazepam), 10 mg/kg, 20 mg/kg, 40 mg/kg and 80 mg/kg ATX for seven days. Thirty min after the administration of the last drug at the indicated doses, PTZ was administered 45 mg/kg to induce an epileptic seizure. The animals were observed for 30 min. Seizure stages according to the Racine Scale (RC) and first myoclonic jerk times (FMJ). Twenty four hours after PTZ injection, passive avoidance test was performed, and then brain tissues were removed for biochemical and histopathological evaluation. The hippocampal Cornu Ammonis 1 (CA1), CA3 and dentate gyrus (DG) regions were evaluated histopathologically regarding neuronal damage. Besides, oxidative stress markers total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI)) were measured in brain tissues. Furthermore, ATX was performed in vitro SH-SY5Y human neuroblastoma cell culture to evaluate PTZ-induced neurotoxicity.Results: When epileptic behaviors were evaluated, ATX did not affect RC and FMJ (p>0, 05). However, ATX reduced both cognitive impairment in passive avoidance test and neuronal damage in the hippocampus (p<0, 05). Moreover, ATX reduced both TOS levels and OSI in the brain (p<0, 05). Besides of these in vitro studies, ATX increased neuronal viability in vitro. Conclusions: Although ATX does not have antiepileptic properties directly, it has a protective effect on not only in vivo but also in vitro. These effects may occur by possible oxidative pathways.
Protective effects of lamotrigine and vitamin B12 on pentylenetetrazole-induced epileptogenesis in rats
(Academic Press Inc Elsevier Science, 2021) Filiz, Ahmet Kemal; Gumus, Erkan; Karabulut, Sebahattin; Tastemur, Yasar; Taskiran, Ahmet Sevki
Epileptogenesis is a process that includes molecular and cellular events that foster the establishment of hyperexcitable neuronal networks in the brain. Pentylenetetrazole (PTZ)-induced kindling model in rodents has added new information to the knowledge about the pathogenesis of epilepsy and potential targets of novel antiepileptic agents. Evidence from animal and human studies suggests that oxidative and inflammatory events may play important roles in the initiation and maintaining seizure activities. Vitamin B12 has beneficial effects on the nervous system and presents pleiotropic effects with antioxidant and anti-inflammatory aspects. In the present study, we aimed to test the hypothesis that vitamin B12 and their combination with lamotrigine prevents behavioral deficits, hippocampal damage, oxidation, and proinflammatory state during epileptogenesis. Male rats were subjected to PTZ-induced epileptogenesis and pretreated with vitamin B12 (50 mu g/kg) or Lamotrigine (LTG) (25 mg/kg) or B12 (50 mu g/kg) + LTG (25 mg/kg). Vitamin B12 and its combination with LTG suppressed epileptogenesis and improved the performance of rats in the passive avoidance test. In addition, Vitamin B12 and its combination with LTG decreased levels of total oxidative status (TOS), oxidative stress index (OSI), interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and increased total antioxidant status (TAS) levels in the hippocampus and cerebral cortex. Furthermore, it reduced hippocampal neuronal damage. Current findings support the beneficial actions of vitamin B12 due to its antioxidative and anti-inflammatory properties during the course of disease. (C) 2021 Elsevier Inc. All rights reserved.
The contribution of non-drug factors to fetal malformation in anti-seizure-medication-treated pregnancy
(Academic Press Inc Elsevier Science, 2021) Filiz, Ahmet Kemal; Gumus, Erkan; Karabulut, Sebahattin; Tastemur, Yasar; Taskiran, Ahmet Sevki
Purpose: To assess the possible contribution of factors in additional to intrauterine anti-seizure medication (ASM) exposure in the occurrence of fetal malformation in women with ASM-treated epilepsy. Results: Logistic regression analysis showed that maternal age over 31 years, family histories of fetal malformation, and conception after assisted fertility treatment, and also dosage of valproate, carbamazepine, and topiramate, made statistically significant (P < 0.05) contributions to the fetal malformation rate in 2223 pregnancies in Australian women with epilepsy. The malformation rates were lower in pregnancies where the non-ASM-associated contributory factors were not present: statistically significantly so for all ASM-exposed pregnancies, and those pregnancies exposed to the more potent teratogenic drugs. Conclusion: It is important to consider the possible roles of identified, and also possible non-identified, non-ASM factors in relation to the occurrence of fetal malformations in the pregnancies of women with ASM-treated epilepsy. (C) 2021 Elsevier Inc. All rights reserved.
The effect of magnesium sulfate on memory and anxiety-like behavior in a rat model: an investigation of its neuronal molecular mechanisms
(Taylor & Francis Ltd, 2024) Cetin, Ali; Ozdemir, Ercan; Golgeli, Asuman; Taskiran, Ahmet Sevki; Karabulut, Sebahattin; Ergul, Mustafa; Gumus, Erkan
BackgroundAnxiety is an adaptive response to potentially threatening conditions. Excessive and uncontrolled anxiety responses become nonadaptive and cause anxiety disorders. To better understand the anxiety-modulating effects of Mg sulfate, behavioral test batteries in the assessment of anxiety and learning and memory functions were performed simultaneously over a time period. This study also examines the effects of Mg sulfate compared to diazepam, an anxiolytic drug with amnestic effects on anxiety-like behavior, as well as possible oxidative-nitrosative stress and hippocampal changes in male rats exposed to predator odor.MethodsYoung adult Sprague-Dawley male rats were used. The rats were assessed using a comprehensive neurobehavioral test battery consisting of novel object recognition, open field, and successive alleys tasks. Anxiety was induced by cat odor, and diazepam and Mg were used as study drugs. Of the frontal cortex and hippocampus, the state of total oxidant and antioxidant and NO levels and histological examination of hippocampal CA1, CA2, CA3, and DG regions were performed.ResultsDiazepam- and Mg-treated rats showed an improvement in anxiety-related behavior to predator odors. Furthermore, Mg treatment alleviated some of the increasing oxidative stress in the frontal cortex and hippocampus of rats, while diazepam treatment in particular enhanced hippocampal oxidant and antioxidant activity. In addition, brain NO increase induced by animal odor exposure or diazepam treatment was ameliorated by Mg administration.ConclusionsOverall, our work suggests that Mg had a partial anxiolytic effect on anxiety-like behaviors, although not as much as diazepam, and this effect varied depending on the dose. Mg treatment might counteract increased oxidative stress and elevated NO levels in the brain.
The effect of penicillin-induced epileptiform activity on proinflammatory cytokines levels in the rat brain
(2021) Filiz, Ahmet Kemal; Karabulut, Sebahattin
Emerging evidence indicates a pathogenic role of protracted neuroinflammation in the various neurodegenerative diseases, including epilepsy. Neuroinflammation may contribute to neuronal hyperexcitability underlying seizure formation. The current research aims to examine the changes in the levels of proinflammatory cytokines such as interleukin-1? (IL-1?) and tumor necrosis factor-? (TNF-?) in the penicillin epilepsy model. In the present study, 12 male Wistar albino rats were randomly divided into two groups as sham and penicillin epilepsy model. Seizures were induced with the intracortical (i.c.) single microinjection 500 IU of penicillin-G into neocortex. Rats were decapitated after observing the cortical epileptic activity and brains were removed by craniotomy. Proinflammatory cytokines (TNF-? and IL-1?) were measured by using ELISA methods in the cortical and hippocampal brain regions. Penicillin significantly up-regulated the expression of IL 1? and TNF-? in the rat cortex, but did not affect the hippocampal cytokines levels. This study is indicative of the neuroinflammatory potential of cortical penicillin administration.
Ursodeoksikolik Asit’in Farelerde Pentilentetrazol ile Oluşturulan Akut Epileptik Nöbetler Üzerine Etkisinin Araştırılması
(2020) Karabulut, Sebahattin; Taşkıran, Ahmet Şevki
Bu çalışmanın amacı, Ursodeksikolik asit (UDKA) ön tedavisinin pentilentetrazol (PTZ) ileindüklenen akut epilepsi fare modelinde nöbet davranışına ve hipokampal total oksidan status(TOS) ve kaspaz-3 düzeylerine etkisini araştırmaktır. Çalışmada BALB-c türü 24 hayvan rastgele4 gruba ayrıldı: Kontrol grubu, PTZ; PTZ ile nöbet indüklenen grup, UDKA-100; 5 gün boyuncaUDKA 100 mg kg-1verilen ve PTZ uygulanan grup, UDKA-200; 5 gün boyunca UDKA 200 mgkg-1verilen ve PTZ uygulanan grup. UDKA ön tedavisinin nöbet davranışı üzerine istatistikselolarak anlamlı bir etkisi bulunmadı. UDKA-200 grubunda daha belirgin olmak üzere, UDKA öntedavisi hipokampal TOS düzeyini anlamlı olarak azalttı. Benzer şekilde, hipokampal kaspaz-3düzeyi UDKA alan gruplarda daha düşük bulundu. Sonuç olarak, UDKA antioksidatif veantiapoptotik özellikleriyle epilepsi tedavisi için faydalı bir terapötik ajan olabilir.
Wi-Fi decreases melatonin protective effect and increases hippocampal neuronal damage in pentylenetetrazole induced model seizures in rats
(MDPI, 2019) Akkaya, Recep; Gümüş, Erkan; Akkaya, Birnur; Karabulut, Sebahattin; Gülmez, Kader; Karademir, Mustafa; Taştemur, Yaşar
Aim: Epilepsy is a common brain disorder in which the seizures could cause a neuronal loss in the hippocampus. Oxidative stress has an important role in the pathology of epilepsy. Some studies indicate that Wi-Fi increases oxidative stress and suppresses antioxidant systems. The aim of this study is to investigate the effect of Wi-Fi on melatonin anticonvulsive effect and oxidative damage in pentylenetetrazole-induced epileptic seizures in rats. Methods: In our study, we used 30 male Wistar Albino rats, 230?250 grams of the body weight. The animals were divided into five groups as control, saline (1 ml/kg/day olive oil for 30 days), Wi-Fi (12 h/day for 30 days), melatonin (10 mg/kg/day for 30 days) and melatonin + Wi-Fi (10 mg/kg/day +12 h/day for 30 days). In the thirtieth day, thirty minutes after the last drugs administration at the indicated doses, PTZ in 45 mg/kg was administered to induce epileptic seizure. The animals were observed for 30 min during the seizure stages (according to the Racine Scale) and first myoclonic jerk times (FMJ). Twenty-four hours after PTZ injection, brain tissues were removed for biochemical and histopathological evaluation. The hippocampal Cornu Ammonis (CA) 1, CA3 and DG (dentate gyrus) regions were histopathologically evaluated in terms of a neuronal damage in addition that oxidative stress markers (total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI)) were measured in brain tissues. Results: Wi-Fi was not found to affect behavioral changes associated with epilepsy (p > 0.05). However, Wi-Fi reduced anticonvulsive and antioxidant effect of melatonin (p < 0.05). Moreover, Wi-Fi increased neuronal damage in hippocampus (p < 0.05). Conclusion: Wi-Fi did not directly affect epileptic seizures. Nevertheless, it inhibits the positive effects of melatonin on epilepsy and it also has negative effects on hippocampal neuronal damage. These effects of Wi-Fi may occur via oxidative pathways. © 2019 Elsevier B.V.

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