| Project/Area Number |
05680685
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | Department of Physiology, School of Medicine, Fujita Health University |
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Principal Investigator |
NAGATA Yutaka Department of Physiology, School of Med., Fujita Health Univ.Prof., 医学部, 教授 (70084499)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAUCHI Masamitsu Dept of Physiol., School of Med., Fujita Health Univ.Instructor, 医学部, 助手 (30278303)
ANDO Masato Dept of Physiology, School of Med., Fujita Health Univ.Instructor, 助教授 (40097720)
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| Project Period (FY) |
1993 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1995: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1994: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1993: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | synaptic transmission / transglutaminase / neurotransmitter (carbachol) / nitric oxide / cyclic GMP / スーパーオキシド・ジムスターゼ(SOD) / 神経伝達物質(カルバコール / 一酸化窒素 / 神経伝達物質 / 脱分極と過分極 |
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| Research Abstract |
Superior cervical sympathtic ganglion (SCG) contains many cholinergic synapses, and maintains impulse transmission activity after removal from the rat. When neurotransmitter (acetylcholine ; Ach) was applied to the physiological saline medium during aerobic incubation of the excised SCG,rapid and significant rise in activity of Ca^<2+> -dependent eNzyme, transglutaminase (TG) was observed. Carbachol, a muscarinic ACh agonist, strongly increased the tissue TG activity within minutes, which was fairly antagonized by a muscarinic ACh antagonist, atropine. Nitric oxide (NO), a new transmitter candidate, remarkably accelerated TG activity in the SCG,and the activity was suppressed by a specific inhibitor for NO synthase, N^G -monomethyl-L-arginine. The rate of NO activation was measured byh the formation of cyclic GMP,but the an inhibitor of guanylate cyclase, methylene blue, did not supressed the Carb-induced TG activity increase. These results suggest that Carb -stimulation to the SCG neurons initiate the intracellular signal transfer process for the activation of TG via receptor mediated NO and cyclic GMP increase to cause intracellular Ca^<2+> rise.
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