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HOME > J Pathol Transl Med > Volume 30(12); 1996 > Article
Original Article Morphological Study on the Mechanism of the Central Nervous System Dysfunction Induced by Unipolar Pulsating Magnetic Field in Mice.
Ro Hyun Sung, Gyeong Hoon Kang, Chong Heon Lee, Suk Keun Lee, Young Hae Chung, Yoo Hurn Suh, Jeong Wook Seo, Je G Chi
Journal of Pathology and Translational Medicine 1996;30(12):1073-1082
DOI: https://doi.org/
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1Department of Pathology, Seoul National University College of Medicine, Seoul, Korea.
2Department of Pharmacology, Seoul National University College of Medicine, Seoul, Korea.

The morphologic change of the mouse brain after exposure to magnetic field is studied. Our magnetic field model was a pulsed unipolar magnetic field with the flux density of 0.2 - 0.3 tesla and the frequency of 60 hertz. Twelve adult male mice were exposed to the magnetic field for 2, 4, 8, 12, 18 and 24 hours. After the exposure to the magnetic field mice were anesthetized with chloral hydrate, and paraformaldehyde was infused through the left ventricle for fixation. During exposure to the magnetic field, behavioral and weight changes of mice were observed. Mice became irritable and restless, especially during first 2 hours of the exposure. Microscopic and ultrastructural examination on the brain revealed nuclear chromatin clumping of the neuron in mice exposed to the magnetic field for more than four hours. The change was proportional to the exposed time and more prominent in the cerebral cortex. An immunohistochemical study for amyloid precursor protein (APP) was also performed. There was an increased expression of APP in the neuronal cytoplasm of the mouse brain exposed to the magnetic field for 4 hours or more. But the reaction was not proportional to the exposure time and reactive neuron was diffusely distributed through the whole brain. Anti-APP antibody reactivity was not correlated with the chromatin clumping. The mechanism of APP induction was postulated as stress-induced APP-gene induction, and the role of APP was presumed to protect the neuron against hazardous environment.

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