| Project/Area Number |
24500434
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | Yamagata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
YAMAZAKI Yoshihiko 山形大学, 医学部, 准教授 (10361247)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2012: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | adenosine / synaptic plasticity / LTP / LTD / hippocampus / NMDA receptors / adenosine A1 receptors / frequency / depotentiation / NMDA receptor / adenosine A1 receptor / astroglia / interneuron / CA1 / シナプス可塑性 / アデノシン受容体 / 海馬 |
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| Outline of Final Research Achievements |
We studied the effects of adenosine A1 receptors (ADOA1Rs) on the synaptic plasticity in CA1 neurons. In the presence of 100 nM adenosine, we found that a tonic inhibition of interneurons for CA1 pyramidal neurons was decreased. Both potentiation and depression of the synaptic response were induced in CA1 neurons by systematically varying the frequency of low frequency afferent stimulation (LFS) between 1-10 Hz and the pulse number between 40-1000. A pharmacological study indicated that, despite their opposite effects, both the synaptic depression induced by LFS at 1 Hz and the synaptic potentiation induced by LFS at 10 Hz were triggered by co-activation of NMDARs, mGluRs and ADOA1Rs at CA1 synapses. We suggest that activation of ADOA1Rs in inhibitory interneurons suppresses the tonic inhibition for CA1 pyramidal neurons, facilitates NMDARs activation during LFS and triggers the mechanism for the bidirectional synaptic plasticity induced in CA1 neurons by 1-10 Hz LFS.
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