Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/933
Title: Response of hippocampal neurons and glial cells to alternating magnetic field in gerbils submitted to global cerebral ischemia
Authors: Rauš, Snežana
Selaković, Vesna
Manojlović-Stojanoski, Milica
Radenović, Lidija 
Prolić, Zlatko
Janać, Branka
Keywords: 50 Hz magnetic field;Animal model;Hippocampus;Histology;Stroke
Issue Date: 1-Jan-2013
Journal: Neurotoxicity Research
Abstract: 
The purpose of this study was to determine whether exposure to an extremely low-frequency magnetic field (ELF-MF, 50 Hz) affects the outcome of postischemic damage in the hippocampus of Mongolian gerbils. After 10-min bilateral carotid occlusion, the gerbils were continuously exposed to ELF-MF (average magnetic induction at the center of the cage was 0.5 mT) for 7 days. The impact of ELF-MF was estimated immediately (the 7th day after reperfusion) and 7 days after cessation of exposure (the 14th day after reperfusion) compared with ischemic gerbils without ELF-MF exposure. Applying stereological methods, histological evaluation of changes in the hippocampus was done for determining its volume, volume densities of degenerating neurons and astrocytes, as well as the number of microglial cells per unit area. ELF-MF per se did not induce any morphological changes, while 10-min global cerebral ischemia led to neuronal death, especially in CA1 region of the hippocampus, as expected. Ischemic gerbils exposed to ELF-MF had significantly a lower degree of cell loss in the examined structure and greater responses of astrocytes and microglial cells than postischemic gerbils without exposure on the seventh day after reperfusion (immediate effect of ELF-MF). Similar response was observed on the 14th day after reperfusion (delayed effect of ELF-MF); however, differences in measured parameters were low and insignificant. Applied ELF-MF has possible neuroprotective function in the hippocampus, as the most sensitive brain structure in the model of global cerebral ischemia, through reduction of neuronal death and activation of astrocytes and microglial cells. © 2012 Springer Science+Business Media, LLC.
URI: https://biore.bio.bg.ac.rs/handle/123456789/933
ISSN: 1029-8428
DOI: 10.1007/s12640-012-9333-8
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