Project/Area Number |
10670090
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
General pharmacology
|
Research Institution | Kumamoto University |
Principal Investigator |
TOKUTOMI Nofumi Kumamoto University, Pharmacology, Associate Professor, 医学部, 助教授 (30227582)
|
Co-Investigator(Kenkyū-buntansha) |
TOKUTOMI Yoshiko Kumamoto University, Pharmacology, Assistant Professor, 医学部, 助手 (90253723)
NISHI Katsuhide Kumamoto University, Pharmacology, Professor, 医学部, 教授 (00040220)
|
Project Period (FY) |
1998 – 1999
|
Project Status |
Completed (Fiscal Year 1999)
|
Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥2,000,000 (Direct Cost: ¥2,000,000)
|
Keywords | anti c-KIT monoclonal antibody (ACK2) / neurite elongation / synaptic formation / patch-clamp technique / hippocampus / cortex / AMPA / kainate receptor-mediated excitatory postsynaptic currents / 脊髄後根神経節細胞 / 抗 c-KIT モノクローナル抗体 / kainate型シナプス活動 |
Research Abstract |
To clarify the roles of c-KIT on the development in synaptic function and CaィイD12+ィエD1 signaling in the mouse brain, we chronically treated new-born BALB/c mice with anti c-KIT monoclonal antibody (ACK2) and investigated the neuronal responses to aminoacid neurotransmitters. The patch-clamp technique was applied to freshly dissociated brain neurons and those in primary culture. In the experiments with freshly dissociated neurons from cortex, hippocampus, cerebellum and hypothalamus with proteases, there was no great difference between control and ACK2-treated mice in both excitatory and inhibitory amino acid-induced membrane currents. In the primary culture with those neurons from above brain regions, ACK2 inhibited elongation of neurites and synaptic formation. This was accompanied by marked reduction in the activity of AMPA/kainate type glutamate receptor-mediated excitatory postsynaptic currents (EPSCs). These results suggest that c-KIT plays important roles in the recovery procedure of neuronal connections after the events of neurotrauma by its stimulating effect on neurite elongation and synaptic formation.
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