| Budget Amount *help |
¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2000: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Research Abstract |
The effects of nicotinic acethylcholice receptor stimulation on neuronal tissue were investigated using primary cultured cells. The addition of methylcarbamylcholine, a nicotinic receptor agonist, increased intracellular calcium level in rat cultured astrocytes. This elevation was completely blocked by the simultaneous addition of hexamethonium, a nicotinic receptor antagonist. Intracellular calcium elevation by methylcarbamylcholine was also observed in calcium-free medium, indicating that the methylcarbamylcholine-induced calcium elevation was mediated by nicotinic receptor stimulation and the source of calcium seems to be intracellular calcium storage. We also investigated the effect of methylcarbamylcholine on rat cultured microglia. The LPS-induced NO and TNF-α release from microglia was not altered by the addition of methylcarbamylcholine. In our cultured microglia, DNA fragmentation was induced by the addition of Cl-adenosine, an unselective adenosine receptor agonists. Methylcarbamylcholine did not induce apoptosis in cultured microglia by itself, however, the addition of methylcarbamylcholine enhanced apoptosis induced by Cl-adenosine. These results suggest that glial cells responds to nicotine via nicotinic receptors and the inflammatory response mediated by activated microglia may be inhibited by nicotinic receptor stimulation.
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