| Co-Investigator(Kenkyū-buntansha) |
HIRAYAMA Eiichi OSAKA CITY UNIV. MED. SCHOOL, Assistant, 医学部, 助手 (40199104)
MUI Koji OSAKA CITY UNIV. MED. SCHOOL, Assistant, 医学部, 助手 (20219835)
FURUTSUKA Daisuke OSAKA CITY UNIV. MED. SCHOOL, Assistant, 医学部, 助手 (70199438)
ONISHI Hiroshi OSAKA CITY UNIV. MED. SCHOOL, Lecturer, 医学部, 講師 (70094464)
YAMAGAMI Sakae OSAKA CITY UNIV. MED. SCHOOL, Assistant Professor, 医学部, 助教授 (20047004)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1989: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1988: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Research Abstract |
Polysomal messenger RNAs (mRNA) isolated from four parts of brain such as cerebrum, diencephalon, pons and medulla oblongata, and cerebellum were incubated with [^<35>S]-methionine in rabbit reticulocyte lysate system. After the incubation, translation products were analyzed by two dimensional gel electrophoresis. There were twenty proteins, in which protein P of El mice was more labeled in cerebellum than in other parts, but less than that of ddY mice. Comparison of translation products of mRNA from whole brain indicated that labeled protein P significantly decreased immediately after the seizures and after 30 min it restored to normal level. These results suggest that mRNA regulated protein P synthesis is associated with seizure-diathesis.
In the synaptic plasma membranes of El mice, ^<32>P incorporation into proteins of molecular weights 200K in cortex and 15OKd in hippocampus was markedly stimulated by combined calcium and calmodulin, whereas it showed a significant inhibition of 20OKd, 10OKd, and 2OKd proteins in amygdala, and 2OKd in hippocampus. The difference of Ca^<2+>-calmodulin kinase II activity between El and ddY mice was remarkable in both hippocampus and amygdala, less pronouns in cortex, and not significant in septa, striatum, thalamus and cerebellum. Thus, hippocampus and amygdala may be responsible for induced-seizure of this animal. Further experiments are need to investigate mRNA species coding for protein P or Ca^<2+>-calmodulin kinase II, and the molecular cloning of cDNA probes being specific relative to such proteins will provide a basis to elucidate the epileptogenesis.
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