2002 Fiscal Year Final Research Report Summary
Molecular mechanisms of error siganl-induced synaptic plasticity related to bird song learning
| Project/Area Number |
13680878
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neuroscience in general
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| Research Institution | DOKKYO UNIVERSITY SCHOOL OF MEDICINE |
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Principal Investigator |
SAKAGUCHI Hironobu Dokkyo University School of Medicine, Physiology, Associate Professor, 医学部, 助教授 (30162291)
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| Project Period (FY) |
2001 – 2002
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| Keywords | Bengalese finch / Zebra finch / Song learning / Protein kinase C / Auditory feedback / Song control nuclei / Synaptic plasticity / Error signal |
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| Research Abstract |
1. An output signal (error signal) from the anterior forebrain pathway in songbird is essential for juvenile song learning and adult song maintenance. In adult Bengalese finches, song patterns remarkably alter after deafening, remain unstable, then stabilize, similarly to the song acquisition in young. In parallel with the song alteration, expression of PKC, considered a molecular marker of synaptic plasticity, increased transiently after deafening, and then decreased gradually in the RA. We lesioned unilaterally the IMAN, which projects to the RA. Following a week, we then deprived them of auditory input by cochlear removal. The immunoreactivity of PKC β1, a subtype of PKC, increased in the RA of intact hemisphere at 2 weeks after deafening. However, in the RA of the lesioned side, PKC immunoreactivity was less intense than that of the non-lesioned side. Namely, the deafened-induced PKC expression was suppressed by the lesion of IMAN. These results suggest that the error signal induces the increase of PKC activity in the RA related to the plasticity of song alterations.
2. In order to clarify the molecular mechanism of error signal-induced PKC activation, two experiments were carried out. First, Ca^<2+> concentration was measured in the brain slice preparation of zebra finch using the fluorescent Ca^<2+> indicator FURA-2-AM. Glutamate caused an increase of intracellular Ca^<2+> concentration in RA neurons. This increase was inhibited by the NMDA receptor antagonist, AP5. Second, we examined the PKC expression in the RA slice preparation after glutamate stimulation for 10 min using PKCβ1 immunohistochemistry. Consequently, glutamate induced the activation of PKC by the translocation from cytosol to membrane. These results indicate that the translocation of the PKC by intracellular Ca^<2+> elevation through NMDA receptor is concerned in the initial stage of error signal-induced-plasticity in RA.
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Research Products
(4 results)
