Project/Area Number |
13672326
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
医薬分子機能学
|
Research Institution | University of Shizuoka |
Principal Investigator |
TAKEDA Atsushi University of Shizuoka, Department of Medical Biochemistry, Associate Professor, 薬学部, 助教授 (90145714)
|
Project Period (FY) |
2001 – 2003
|
Project Status |
Completed (Fiscal Year 2003)
|
Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥1,200,000 (Direct Cost: ¥1,200,000)
|
Keywords | zinc / manganese / iron / brain / hippocampus / essential trace metal / glutamatergic neuron / neurological disease / 扁桃体 / シナプス神経伝達 / カドミウム / シナプス / 学習 / 脳腫瘍 / 画像診断 |
Research Abstract |
Trace metals such as zinc, manganese and iron are necessary for the growth and functions in the brain. The transport of trace metals into the brain is strictly regulated by the brain barrier system, i.e., the blood-brain and blood-cerebrospinal fluid barriers. The alteration of homeostasis of trace metals in the brain is associated with brain diseases. Trace metals usually serve the function of metalloproteins in neurons and glial cells, while a portion of trace metals exist in the presynaptic vesicles, and may be released with neurotransmitters into the synaptic cleft. Zinc and manganese influence the concentration of neurotransmitters in the synaptic cleft, probably via the action against neurotransmitter receptors and transporters and ion channels. Zinc may be an inhibitory neuromodulator of glutamate release in the hippocampus. Dietary zinc deficiency affects zinc homeostasis in the brain followed by an enhanced excitotoxicity of glutamate in the hippocampus. Transferrin may be involved in the transport of iron and manganese into the brain and their utilization there.
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