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    Evaluation of neuroprotection by melatonin against adverse effects of prenatal exposure to a nonsteroidal anti-inflammatory drug during peripheral nerve development
    (PERGAMON-ELSEVIER SCIENCE LTD, 2015) Keskin, Ilknur; Kaplan, Suleyman; Kalkan, Serpil; Sutcu, Mustafa; Ulkay, M. Basak; Esener, O. Burak
    The potential ability of melatonin to protect against impairment of the fetal peripheral nerve system due to maternal consumption of diclofenac sodium (DS) was investigated. Eighty-four pregnant rats were divided into seven groups: control (CONT), saline administered (PS), DS administered (DS), DS with low-dose melatonin administered (DS + MLT10), DS with high-dose melatonin administered (DS+MLT50), low-dose melatonin administered (MLT10), and high-dose melatonin administered (MLT50). After the pregnancy, six male newborn rats from each group were sacrificed at 4 and 20 weeks of age. Their right sciatic nerves were harvested, and nerve fibers were evaluated using stereological techniques. Mean numbers of myelinated axons, axon cross-section areas and the mean thickness of the myelin sheet were estimated. Four-week-old prenatally DS-exposed rats had significantly fewer axons, a smaller myelinated axonal area, and a thinner myelin sheath compared to CONT group (p < 0.05). Although melatonin at both doses significantly increased axon numbers, only a high dose of melatonin increased the diameter of those axons (p < 0.05). At 20-weeks of age, myelinated axon number in the DS group was not only significantly lower than all other groups (p < 0.05) but also the cross-sectional area of these axons was smaller than all other groups (p < 0.05). There were no differences between the groups regarding the mean thickness of the myelin sheet. The current study indicates that prenatal exposure to DS decreases the number and the diameter of sciatic nerve axons and that melatonin prophylaxis can prevent these effects. (C) 2014 Elsevier Ltd. All rights reserved.
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    Hippocampal cell loss after an anterior and posterior anastomotic vein occlusion model in rats
    (PERGAMON-ELSEVIER SCIENCE LTD, 2011) Aydin, Keramettin; Cokluk, Cengiz; Ayas, Bulent; Onger, Mehmet Emin; Keskin, Ilknur; Ozyasar, Ali; Aslan, Huseyin
    Estimation of the cell number after cortical venous ischemia/infarction induced by anterior and posterior anastomotic veins occlusion in a rat model is very important. Twenty male Sprague-Dawley rats were used in this experiment. Small burr-holes were made over the anterior (the crossing point of the line drawn from the posterior border of the orbital rim and the line drawn along the para-midline to the superior sagittal suture) and posterior (just inferior point of the posterior ending of the zygomatic arch) anastomotic veins. Bipolar coagulation technique and micro-scissor were used to sacrifice the venous vessels after final inspection and description. Specimens were evaluated by histopathological and unbiased stereological methods for microscopic evaluation and volumetric analysis, respectively. Significant cell loss was seen in the pyramidal and granule cells of the cornu ammonis and dentate gyrus of the hippocampus after venous ischemia. Cell loss was also pronounced when seen in the histological examination. The present results suggest that the sacrifice of anterior and posterior anastomotic veins can be used as an experimental rat model in the evaluation of pyramidal and granule cell loss in the hippocampus that often assesses the neural damage inflicted by this intervention. (C) 2011 ISDN. Published by Elsevier Ltd. All rights reserved.