Person: GÜLHAN, REZZAN
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GÜLHAN
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REZZAN
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Publication Open Access The effects of partial bilateral lesioning of substantia nigra in a genetic absence epilepsy rat model(2002-04-01) GÜLHAN, REZZAN; ONAT, FİLİZ; GÖREN, MEHMET ZAFER; GÖREN M. Z., GÜLHAN R., ONAT F., Ergün A.Objective: \"Genetic Absence Epilepsy Rats from Strasbourg\" (GAERS), an inbred Wistar strain, serve as an experimental venue. These rats generate spontaneous spike-and-wave discharges (SWD) and have increased γ-aminobutyric acid (GABA) levels in the ventrolateral thalamus (VLT). Recently, substantia nigra pars reticulata (SNpr) was reported to act as an endogeneous inhibitory mechanism in the generation, onset and maintenance of various types of seizures. The presence of tonic control exerted by SNpr in absence seizures should also be tested in GAERS. Methods: In this current study, GABA and L-glutamic acid release in VLT of GAERS with partial bilateral electrolytic lesions of SNpr was evaluated by using microdialysis technique with fluorescent detection. Results: GABA levels in VLT were 0.12±0.04 μM and 0.24±0.08 μM in sham-lesioned and SNpr-lesioned GAERS, respectively. L-glutamic acid level was found to be 0.41 5±0.150 μM in sham-lesioned group and 0.324±0.094 μM in SNpr-lesioned GAERS. Statistical analysis revealed no significant difference between sham-lesioned and SNpr-lesioned rats. The number and the duration of SWD were also similar in two groups. Conclusion: These findings show that SNpr does not exert a tonic control in GAERS and we assume that intact SNpr acts as a site that may exert an inhibition on target structures when activated in GAERS.Publication Metadata only Perirhinal cortical kindling in rats with genetic absence epilepsy(ELSEVIER IRELAND LTD, 2010) ONAT, FİLİZ; Akman, Ozlem; Karson, Ayse; Aker, Rezzan Gulhan; Ates, Nurbay; Onat, Filiz YilmazTwo genetic models of absence epilepsy, GAERS and WAG/Rij rat strains, are resistant to progression of partial seizures induced by amygdaloid or hippocampal kindling. Perirhinal cortex is one of the crucial areas for the secondary generalization of partial seizures. Therefore we focused on perirhinal cortical kindling in both epileptic rat strains and examined whether the resistance to limbic epilepsy is restricted to the amygdala and hippocampus or whether it can also occur with perirhinal cortical kindling. The mean afterdischarge (AD) thresholds were significantly higher in WAG/Rij and GAERS compared to the Wistar rats. Analysis of the rate of perirhinal cortical kindling for the 3 strains indicated highly significant differences. The mean number of stimulations for the development of the first stage 2, 3, 4 or 5 seizures was significantly higher in WAG/Rij and GAERS groups than in Wistar rats. Further, the cumulative total duration and number of SWDs increased during the first epoch of the post-stimulation period at the first stage 2 and 4/5 seizures in the WAG/Rij and GAERS rats compared to the pre-stimulation period. The higher AD threshold and delays to all stages of kindling in WAG/Rij and GAERS indicate that the perirhinal cortex is a part of the circuits involved in the kindling resistance in genetic models of absence epilepsy. (C) 2010 Elsevier Ireland Ltd. All rights reserved.Publication Metadata only Increased inhibitory synaptic activity in the hippocampus (CA1) of genetic absence epilepsy rats: Relevance of kindling resistance(ELSEVIER, 2016) ONAT, FİLİZ; Carcak, Nihan; Dilekoz, Ergin; Gulhan, Rezzan; Onur, Rustu; Onat, Filiz Yilmaz; Sara, YildirimPurpose: Genetic absence epilepsy rats from Strasbourg (GAERS), a well-validated genetic rat model for typical absence epilepsy, are known to manifest a resistance to secondary generalization of abnormal focal electrical activity evoked by kindling. The mechanism of this resistance is still unclear. In order to understand the possible mechanism of kindling resistance, we investigated for the first time, the differences of short-term synaptic plasticity by using a paired-pulse paradigm as an indicator of GABAergic activity in CM region of hippocampus in GAERS and non-epileptic Wistar rats in-vivo. Methods: Rats were subjected to kindling process, basolateral amygdala was stimulated twice a day, with a supra-threshold current, until they displayed limbic or convulsive seizures. One hour after the last kindling stimulation, evoked field potentials from CA1 pyramidal layer of hippocampus were recorded in-vivo under urethane anesthesia. Results: In response to supra-threshold kindling stimulations GAERS showed a significantly delayed kindling progression and displayed a significant increase in hippocampal excitability at early stages of kindling that is the critical for the development of convulsive seizures. In control rats that were not received kindling stimulation, paired-pulse depression (PPD) was significantly pronounced in GAERS with respect to the Wistar group. During the kindling course, PPD was gradually reduced in the Wistar rats as kindling progression was advanced. However in GAERS, PPD ratios were not significantly changed at early stages of kindling. When GAERS reached convulsive stage, their PPD ratios became similar to that of Wistar rats. Discussion: The increased inhibition in paired-pulse responses at early stages of kindling in GAERS suggests the role of augmented GABAergic activity as one of the underlying mechanisms of kindling resistance observed in genetic rat models of absence epilepsy. (C) 2016 Published by Elsevier B.V.