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donderdag, 22 oktober 2009 - Categorie: Onderzoeken
Gerelateerd artikel: en.wikipedia.org/wiki/Synaptic_vesicle
Bron: Synapse (New York) 2009 Nov; 63(11):1010-6.
Abnormality of synaptic vesicular associated proteins in cerebral cortex and hippocampus after microwave exposure.
Wang L, Peng R, Hu X, Gao Y, Wang S, Zhao L, Dong J, Su Z, Xu X, Gao R, Lei C.
Beijing Institute of Radiation Medicine, 27 Taiping Road, Beijing 100850, People's Republic of China.
Studies were performed to determine the effects of microwave on synaptic vesicles and the expression of synaptic vesicular associated proteins including synapsin I, VAMP-2, syntaxin, and synaptophysin. 25 Wistar rats were exposed to microwave which the average power density was 30 mW/cm(2), and whole body average specific absorption rate was 14.1 W/kg for 5 min.
Synaptosome preparations in the cerebral cortex and hippocampus were obtained by isotonic Percoll/sucrose discontinuous gradients at 6 h, 1, 3, and 7 days after radiation.
The expression of synaptic vesicular associated proteins was measured using Western blots and image analysis. The interaction between VAMP-2 and syntaxin was examined by coimmunoprecipitation analysis. Synapsin I in the cerebral cortex were decreased at 3 days (P < 0.01) after radiation and in the hippocampus increased at 1 day (P < 0.01), decreased at 3 days (P < 0.01), increased again at 7 days (P < 0.01) after exposure, compared with the sham-treated controls. Synaptophysin were increased in 1-7 days (P < 0.01) after exposure in the cerebral cortex and hippocampus. VAMP-2 were decreased at 1 and 3 days (P < 0.01) and syntaxin were decreased in 6 h to 3 days (P < 0.01) after radiation in the cerebral cortex and hippocampus. The interactions between VAMP-2 and syntaxin were decreased at 3-7 days (P < 0.01) after radiation in the cerebral cortex and hippocampus, compared with the sham-treated controls.
These results suggest that 30 mW/cm(2) (SAR 14.1 W/kg) microwave radiation can result in the perturbation of the synaptic vesicles associated proteins: synapsin I, synaptophysin, VAMP-2, and syntaxin. The perturbation could induce the deposit of synaptic vesicle, which might be relative to the dysfunction of the synaptic transmission, even the cognition deficit.
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