|Budget Amount *help
¥3,600,000 (Direct Cost : ¥3,600,000)
Fiscal Year 2004 : ¥500,000 (Direct Cost : ¥500,000)
Fiscal Year 2003 : ¥600,000 (Direct Cost : ¥600,000)
Fiscal Year 2002 : ¥2,500,000 (Direct Cost : ¥2,500,000)
We investigated the following studies (Exps.1-4), using both sodium nitroprusside(SNP) and L-arginine(Arg) as NO donor, which increase the level of NO in the brain, and aminoguanidine(AG) as an inhibitor of NO syntase(NOS), which decreases the NO level ; Exp1,Effects of NO levels on the circadian rhythm of locomotor activity in diabetic and non-diabetic rats ; Exp.2,Effects of NO levels on spontaneous locomotor activity in type 2 diabetic mice ; Exp.3,Effects of NO levels on monoamine levels in hippocampus of type 1 diabetic and non-diabetic rats, using in vivo microdialysis techniques ; Exp.4,Effects of NO levels on the memory in Alzheimer model rats, using passive shuttle avoidance system. Results : Exp.1;SNP(0.1〜1mM) increased the locomotor activity in dark period (active stage) of only diabetic rats. On the other hand, AG (0.1〜1mM)decreased the locomotor activity in the non-diabetic rats, but increased it in the diabetic rats. Exp.2;SNF and Arg significantly enhanced the spontaneous locomotor activity of mice in a dose-dependent fashion, especially in diabetic mice.Exp.3;SNP (0.01〜1mM) administrated intraperitoneally increased NO level in the hippocampus dose-dependently, especially in diabetic rats. However AG also increased it. Exp.4;In Alzheimer model rats induced by scopolamine (5mg/kg body wt.), SNP (0.1〜10mM) showed the improvement of the memory. There findings suggest that NO levels in the brain influence at least in part on the activation of the brain function.