2010 Fiscal Year Final Research Report
Possible regulation by excitatory signals on GABAB receptor desensitization via AMPK activation.
Project/Area Number |
21790099
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Single-year Grants |
Research Field |
Biological pharmacy
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Research Institution | Setsunan University |
Principal Investigator |
KURAMOTO Nobuyuki Setsunan University, 薬学部, 准教授 (60324092)
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Project Period (FY) |
2009 – 2010
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Keywords | 神経生物学 |
Research Abstract |
The increase in the p783 level, which is AMPK-dependent phosphorylation site on GABA_B receptors R2 subunit, suppresses desensitization of the receptors. The p783 level was increased by NMDA exposure in the primary neurons, which were cultured in DMEM-based medium. On the other hand, the phosphorylation site immediately dephosphorylated in vitro system, according to the decrease in AMPK activity. It is thus suggested that GABA_B receptors functions were promptly regulated by the alteration of AMPK activity.
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