2013 Fiscal Year Final Research Report

Analysis of the pathogenic mechanism for neuropsychiatric disease-like abnormal behavior in IRBIT knockout mouse

Research Project

Project/Area Number	24700389
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Neurochemistry/Neuropharmacology
Research Institution	Institute of Physical and Chemical Research
Principal Investigator	KAWAAI Katsuhiro 独立行政法人理化学研究所, 脳科学総合研究センター, 研究員 (00553653)
Project Period (FY)	2012-04-01 – 2014-03-31
Keywords	IRBIT / 多動障害 / モノアミン / CaMKII / NBC1 / pH
Research Abstract	An IP3R binding protein termed IRBIT (IP3R binding protein released with inositol 1,4,5-trisphosphate) that interacts with the IP3 binding core domain of IP3R and regulate the IP3 sensitivity of IP3R. Recently, we identified calcium/calmodulin-dependent kinase II alpha (CaMKIIalpha) as an IRBIT binding protein. In this study, we investigated the effect of IRBIT deletion on the monoamine (dopamine and norepinephrine) synthesis and intracellular pH regulation to explain the function of IRBIT in the central nervous system. We found that IRBIT regulated the phosphoryaltion state of TH by CaMKIIalpha. In addition, IRBIT contributed the regulation of intracellular pH by NBC1 in the neuron and astrocyte.

(2 results)