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To investigate whether exposure to an extremely low-frequency magnetic field affects the outcome of post-ischemic damage in the hippocampus of Mongolian gerbils.
Cerebral ischemia was induced by surgical occlusion of both common carotid arteries for 10 min. Adult (3-month-old) male gerbils were divided into six groups: 1.) intact controls (n=3), 2.) sham operated (n=6), 3.) sham exposure (n=6), 4.) exposure (n=9), 5.) ischemia + sham exposure (n=9), and 6.) ischemia + exposure (n=9). All groups were subdivided into two groups and histological analyses were performed immediately at the end of exposure (on day 7) and 7 days after cessation of exposure (on day 14), respectively.
Animals were divided into the following groups: i) intact controls ii) sham operated iii) sham exposure iv) exposure v) ischemia + sham exposure vi) ischemia + exposure
|ばく露時間||continuous for 7 days|
|ばく露装置の詳細||two 26 cm x 43 cm x 15 cm cages with 3 - 4 animals placed at either side of the electromagnet so that the cage's center was at 20 cm distance from it|
|Sham exposure||A sham exposure was conducted.|
Exposure to extremely low frequency magnetic fields alone did not induce any morphological changes in the hippocampus, while 10-min global cerebral ischemia led to neuronal death, especially in the CA1 region of the hippocampus.
Ischemic gerbils exposed to extremely low frequency magnetic fields (group 6) had a significantly lower degree of cell loss in the hippocampus and greater responses of astrocytes and microglial cells than post-ischemic gerbils with shamexposure (group 5) at the end of the 7-day exposure period. A similar response was observed on the seventh day after cessation of exposure (day 14, delayed effect); however, differences were low and the results statistically non-significant.
The authors conclude that exposure to extremely low frequency magnetic fields 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.