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    Effect of levetiracetam on penicillin induced epileptic activity in rats
    (Nencki Inst Experimental Biology, 2014) Arik, Aliye Erguvan; Bagirici, Faruk; Sefil, Fatih; Marangoz, Cafer
    The aim of this study was to investigate the effects of levetiracetam (LEV) on penicillin- induced epileptiform activity in rats. Penicillin was applied intracerebroventricularly (icy) at a dose of 500 IU to induce epileptiform activity. LEV was given intraperitoneally (ip) at doses of 20, 40, 80 mg/kg before penicillin injection. This agent reduced epileptiform activity by decreasing spike frequencies. The mean spike frequencies decreased significantly in all the LEV treated groups. There was no significant change in the spike amplitudes of the LEV groups compared with the control group. 40 mg/kg of LEV was determined as the most effective dose on reducing epileptiform activity. The results of this study suggest that LEV is an effective antiepileptic agent in penicillin-induced epilepsy.
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    Influence of carbenoxolone on the anticonvulsant efficacy of phenytoin in pentylenetetrazole kindled rats
    (Nencki Inst Experimental Biology, 2012) Sefil, Fatih; Bagirici, Faruk; Acar, M. Dilek; Marangoz, Cafer
    Abnormal synchronized neuronal discharges mediated by gap junctions have an important role in epileptic seizures. The analysis of anticonvulsant drugs acting on gap junctions is still a priority in epilepsy research. Therefore, the present study was designed to investigate the effect of carbenoxolone, a gap junction blocker, on the anticonvulsant efficacy of phenytoin in pentylenetetrazole kindled rats. Male Wistar albino rats, 14 weeks of age, were used. In the first step of the study, animals were given PTZ 35 mg/kg intraperitoneally (i.p.) three times a week until kindling was produced. Then, indwelling screw electrodes - allowing EEG monitoring of conscious rats - were implanted into the crania of the kindled rats. In this way, we were able to record EEG activity and evaluate seizure stage at the same time. In the second step of the study, the interaction between carbenoxolone (40 mg/kg i.p.) and phenytoin (60 mg/kg, i.p.) was investigated. The data analysis was performed using a one-way ANOVA with LSD post-hoc test. Total spike number and the generalized seizure duration were reduced in the carbenoxolone treated group compared to the PTZ group. Phenytoin decreased generalized seizure duration, total spike number and seizure severity score. Carbenoxolone and phenytoin have anti-seizure effects in PTZ kindled rats. There was no significant difference between the carbenoxolone + phenytoin combination and phenytoin in terms of generalized seizure duration, total spike number and seizure stage. The results indicate that carbenoxolone combined with phenytoin is not more effective than the use of these drugs alone.
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    Seizures with pentylenetetrazol kindling cause a decrease in the number of pyramidal neurons in the rat hippocampus
    (Science Printers and Publishers Inc., 2016) Kocacan, Süleyman Emre; Sefil, Fatih; Elibol, Ebru; Altunkaynak, Berrin Z.; Acar, Meryem Dilek; Bağirici, Faruk; Marangoz, Cafer
    OBJECTIVE: To investigate the effects of pentylenetetrazole (PTZ) kindling on the number of pyramidal neurons in the rat hippocampus. STUDY DESIGN: Using unbiased stereology, we calculated total pyramidal neuron numbers in the CA1, CA2, and CA3 areas and the whole hippocampus after PTZ-induced kindling. The estimation and the analysis of the number of hippocampal pyramidal cells (areas of CA1-3) were done with the optical fractionator technique, which is a stereological counting technique. RESULTS: Stereological analysis showed that the total number of pyramidal neurons in the whole hippocampus and the number of pyramidal neurons in CA1 were significantly lower in kindled rats as compared to the controls (p < 0.05). However, no significant difference was found in the neuron numbers of CA2 and CA3 (p>0.05). CONCLUSION: PTZ-induced seizures cause a decrease in the amount of pyramidal neurons in the CA area of the rat hippocampus. © Science Printers and Publishers, Inc.