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    Effects of neurofeedback therapy in healthy young subjects
    (The Canadian Society for Clinical Investigation, 2016) Altan, Sümeyra; Berberoğlu, Bercim; Canan, Sinan; Dane, Şenol
    Purpose: Neurofeedback refers to a form of operant conditioning of electrical brain activity, in which desirable brain activity is rewarded and undesirable brain activity is inhibited. The research team aimed to examine the efficacy of neurofeedback therapy on electroencephalogram (EEG) for heart rate, electrocardiogram (ECG) and galvanic skin resistance (GSR) parameters in a healthy young male population. Methods: Forty healthy young male subjects aged between 18 to 30 years participated in this study. Neurofeedback application of one session was made with bipolar electrodes placed on T3 and T4 (temporal 3 and 4) regions and with reference electrode placed on PF1 (prefrontal 1). Electroencephalogram (EEG), electrocardiogram (ECG) and galvanic skin resistance (GSR) were assessed during Othmer neurofeedback application of one session to regulate slow wave activity for forty minutes thorough the session. Data assessed before neurofeedback application for 5 minutes and during neurofeedback application of 30 minutes and after neurofeedback application for 5 minutes throughout the session of 40 minutes. Means for each 5 minutes, that is to say, a total 8 data points for each subjects over 40 minutes, were assessed. Results: Galvanic skin resistance increased and heart rate decreased after neurofeedback therapy. Beta activity in EEG increased and alfa activity decreased after neurofeedback therapy. Conclusions: These results suggest that neurofeedback can be used to restore sympathovagal imbalances. Also, it may be accepted as a preventive therapy for psychological and neurological problems.
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    Examination of age-dependent effects of fetal ethanol exposure on behavior, hippocampal cell counts, and doublecortin immunoreactivity in rats
    (Wiley, 2014) Elibol-Can, Birsen; Dursun, İlknur; Telkes, İlknur; Kılıç, Ertuğrul; Canan, Sinan; Jakubowska-Doğru, Ewa
    Ethanol is known as a potent teratogen having adverse effects on brain and behavior. However, some of the behavioral deficits caused by fetal alcohol exposure and well expressed in juveniles ameliorate with maturation may suggest some kind of functional recovery occurring during postnatal development. The aim of this study was to reexamine age-dependent behavioral impairments in fetal-alcohol rats and to investigate the changes in neurogenesis and gross morphology of the hippocampus during a protracted postnatal period searching for developmental deficits and/or delays that would correlate with behavioral impairments in juveniles and for potential compensatory processes responsible for their amelioration in adults. Ethanol was delivered to the pregnant dams by intragastric intubation throughout 7-21 gestation days at daily dose of 6 g/kg. Isocaloric intubation and intact control groups were included. Locomotor activity, anxiety, and spatial learning tasks were applied to juvenile and young-adult rats from all groups. Unbiased stereological estimates of hippocampal volumes, the total number of pyramidal and granular cells, and double cortin expressing neurons were carried out for postnatal days (PDs) PD1, PD10, PD30, and PD60. Alcohol insult during second trimester equivalent caused significant deficits in the spatial learning in juvenile rats; however, its effect on hippocampal morphology was limited to a marginally lower number of granular cells in dentate gyrus (DG) on PD30. Thus, initial behavioral deficits and the following functional recovery in fetal-alcohol subjects may be due to more subtle plastic changes within the hippocampal formation but also in other structures of the extended hippocampal circuit. Further investigation is required. (c) 2013 Wiley Periodicals, Inc. Develop Neurobiol 74: 498-513, 2014
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    Protective effects of melatonin and omega-3 on the hippocampus and the cerebellum of adult Wistar albino rats exposed to electromagnetic fields
    (Elsevier Inc., 2017) Altun, Gamze; Kaplan, Süleyman; Deniz, Ömür Gülsüm; Kocacan, Süleyman Emre; Canan, Sinan; Davis, Devra; Marangoz, Cafer
    The purpose of the study was to investigate the effects of pulsed digital electromagnetic radiation emitted by mobile phones on the central nervous system of the adult Wistar albino rats. The study evaluated structural and functional impacts of four treatment arms: electromagnetic field (EMF) exposed; EMF exposed + melatonin treated group (EMF + Mel); EMF exposed + omega-3 (?3) treated group (EMF + ?3); and control group (Cont). The 12-weeks-old rats were exposed to 900 MHz EMF for 60 min/day (4:00–5:00 p.m.) for 15 days. Stereological, biochemical and electrophysiological techniques were applied to evaluate protective effects of Mel and ?3. Significant cell loss in the CA1 and CA2 regions of hippocampus were observed in the EMF compared to other groups (p < 0.01). In the CA3 region of the EMF + ?3, a significant cell increase was found compared to other groups (p < 0.01). Granular cell loss was observed in the dentate gyrus of the EMF compared to the Cont (p < 0.01). EMF + ?3 has more granular cells in the cerebellum than the Cont, EMF + Mel (p < 0.01). Significant Purkinje cell loss was found in the cerebellum of EMF group compared to the other (p < 0.01). EMF + Mel and EMF + ?3 showed the same protection compared to the Cont (p > 0.05). The passive avoidance test showed that entrance latency into the dark compartment was significantly shorter in the EMF (p < 0.05). Additionally, EMF had a higher serum enzyme activity than the other groups (p < 0.01). In conclusion, our analyses confirm that EMF may lead to cellular damage in the hippocampus and the cerebellum, and that Mel and ?3 may have neuroprotective effects.