Project/Area Number |
10680718
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Neurochemistry/Neuropharmacology
|
Research Institution | Okayama University |
Principal Investigator |
MORIWAKI Akiyoshi Okayama University Medical School, Associate, 医学部, 講師 (10144742)
|
Co-Investigator(Kenkyū-buntansha) |
MATSUI Hideki Okayama University Medical School, Professor, 医学部, 教授 (30157234)
MATSUSHITA Masayuki Okayama University Medical School, Assistant, 医学部, 助手 (30273965)
KONDO Eisaku Okayama University Medical School, Assistant, 医学部, 助手 (30252951)
TOMIZAWA Kazuhito Okayama University Medical School, Assistant, 医学部, 助手 (40274287)
|
Project Period (FY) |
1998 – 1999
|
Project Status |
Completed (Fiscal Year 1999)
|
Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 1999: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1998: ¥2,300,000 (Direct Cost: ¥2,300,000)
|
Keywords | Cyclin-dependent kinase / cdk5 / p35 / Hippocampus / Synaptic vesicle / Synapsin / Actin |
Research Abstract |
Cyclin-dependent kinases have been believed to regulate synaptic transmission. We investigated the contribution of cyclin-dependent kinase 5 (cdk5) on the transmission using hippocampal neurons. Cdk 5 requests a critical regulatory subunit p35 when it exerts enzymatic activity. In the adult rat brain, cdk5 was detected within dendrites and axons, and not detected within perikarya of neurons, However, p35 was detected within the perykarya and not detected at axons nor dendrites. These results indicate that cdk 5 and p35 do not exist concurrently within the neurons, this suggests that the activity of cdk5 is regulated by other activators than p35 at the presynaptic terminals. We further studied the effect of cdk5 on neuronal transmission using hippocampal slices of adult rats. Field excitatory postsynaptic potentials (EPSPs) were recorded from the CA1 region by stimulating Schaffer collateral-commissural fibers. Bath application of roscovitine, which is an inhibitor of cdk5, increased the amplitudes of EPSPs. These results suggest that cdk5 has some rele in regulating transmitter release.
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