| Project/Area Number |
17300125
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurophysiology and muscle physiology
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| Research Institution | Hokkaido University |
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Principal Investigator |
KAMIYA Haruyuki Hokkaido University, Grad. School of Med., Professor (10194979)
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| Co-Investigator(Kenkyū-buntansha) |
KAMIYA Haruyuki Hokkaido University, Grad. School of Med., Professor (10194979)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥16,050,000 (Direct Cost: ¥15,000,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2007: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2006: ¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2005: ¥8,100,000 (Direct Cost: ¥8,100,000)
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| Keywords | HIPPOCAMPUS / SYNAPTIC TRANSMISSION / GLUTAMATE / GABA / GABA |
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| Research Abstract |
Recent studies suggested that hippocampal mossy fiber terminals of young rodents release GABA in addition to glutamate. In this study, we examined the exact cellular mechanisms underlying co-release of GABA and glutamate using whole cell recordings in hippocampal slices as well as immunohistochemistry in young mice (P14-P21). Strong stimulus to the granule cell layer of dentate gyrus reliably elicited IPSCs in CA3 neurons in the presence of glutamate receptor antagonists 10μM CNQX and 25μM D-AP5. These putative monosynaptic IPSCs were abolished by further application of GABA_A receptor antagonist 100μM picrotoxin. In contrast, weak stimulus to the granule cell layer never elicited IPSCs in the presence of CNQX and D-AP5. The differential effects of the glutamate receptor antagonists between strong and weak stimuli suggested that some additional cellular components were recruited by the strong stimulus of the granule cell layer. We also examined localization of GABA and the GABA-synthesizing enzyme GAD immunohistochemically, and found that GABA and GAD were expressed weakly at the mossy fiber terminals. However, vesicular GABA transporter VGAT was not detected within the terminals. These results suggested that strong stimulus to the granule cell layer causes apparent monosynaptic IPSCs by stimulating inhibitory interneurons in addition to mossy fibers, and the hippocampal mossy fiber terminals themselves may not release GABA in young mouse.
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