Functional alterations in immature cultured rat hippocampal neurons after sustained exposure to static magnetic fields.
In cultured rat hippocampal neurons, gradual increases were seen in the expression of microtubule-associated protein-2 (MAP-2), neuronal nuclei (NeuN) and growth-associated protein-43 (GAP-43), in proportion to increased duration, up to 9 days in vitro (DIV). Sustained exposure to static magnetic fields at 100 mT for up to 9 DIV significantly decreased expression of MAP-2 and NeuN in cultured rat hippocampal neurons without markedly affecting GAP-43 expression. Although a significant increase was seen in the expression of glial fibrillary acidic protein (GFAP) in hippocampal neuronal preparations cultured for 6-9 DIV under sustained magnetism, GFAP and proliferating cell nuclear antigen expression were not affected markedly in cultured astrocytes prepared from rat hippocampus and neocortex, irrespective of cellular maturity. No significant alteration was seen in cell survivability of hippocampal neurons or astrocytes cultured under sustained magnetism. In hippocampal neurons cultured for 3 DIV under sustained magnetism, marked mRNA expression was seen for N-methyl-D-aspartate (NMDA) receptor subunits, NR1, NR2A-2C, NR2D, and NR3A. In addition, significant potentiation of the ability of NMDA to increase intracellular free Ca(2+) ions was observed. Differential display analysis revealed a significant decrease in mRNA expression for the transcription factor ALF1 in response to sustained magnetism for 3 DIV. These results suggest that sustained exposure to static magnetic fields may affect cellular functionality and maturity in immature cultured rat hippocampal neurons through modulation of expression of particular NMDA receptor subunits.
Hirai
Takao
T
Laboratory of Molecular Pharmacology, Kanazawa University Graduate School of Natural Science and Technology, Kanazawa, Japan.
Yoneda
Yukio
Y
Laboratory of Molecular Pharmacology, Kanazawa University Graduate School of Natural Science and Technology, Kanazawa, Japan.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D020013:Calcium Signaling / Q000502:physiology / Q000528:radiation effects; D002454:Cell Differentiation / Q000502:physiology / Q000528:radiation effects*; D002478:Cells, Cultured; D004574:Electromagnetic Fields; D005333:Fetus; D019922:GAP-43 Protein / Q000378:metabolism / Q000528:radiation effects; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism / Q000528:radiation effects; D006624:Hippocampus / Q000166:cytology / Q000378:metabolism / Q000528:radiation effects*; D007424:Intracellular Fluid / Q000378:metabolism / Q000528:radiation effects; D008280:Magnetics; D008869:Microtubule-Associated Proteins / Q000378:metabolism / Q000528:radiation effects; D009419:Nerve Tissue Proteins / Q000378:metabolism / Q000528:radiation effects*; D009434:Neural Pathways / Q000254:growth & development / Q000378:metabolism / Q000528:radiation effects*; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism / Q000528:radiation effects; D021122:Protein Subunits / Q000235:genetics / Q000528:radiation effects; D012333:RNA, Messenger / Q000378:metabolism / Q000528:radiation effects; D051381:Rats; D017208:Rats, Wistar; D016194:Receptors, N-Methyl-D-Aspartate / Q000235:genetics / Q000528:radiation effects*
D019922:GAP-43 Protein; D005904:Glial Fibrillary Acidic Protein; D008869:Microtubule-Associated Proteins; D009419:Nerve Tissue Proteins; D018809:Proliferating Cell Nuclear Antigen; D021122:Protein Subunits; D012333:RNA, Messenger; D016194:Receptors, N-Methyl-D-Aspartate; D002118:Calcium