2013 Fiscal Year Final Research Report
The regulatory mechanisms and the physiological significance of SNAP-25 phosphorylation in mouse brain.
| Project/Area Number |
24700385
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | Kitasato University |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Keywords | リン酸化 / 神経伝達物質放出 / ストレス / SNAREタンパク質 / プレシナプス / ドーパミン / SNAP-25 / PKC |
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| Research Abstract |
SNAP-25 plays a crucial role in neurotransmitter release by exocytosis. Protein kinase C phosphorylates SNAP-25 at Ser187, however the physiological significance of this phosphorylation event in brain function remains unclear. We found that SNAP-25 phosphorylation increased rapidly in the mouse brain following cold-water restraint stress. Both basal and stress-induced phosphorylation of SNAP-25 were high in stress-related brain regions and the extent of phosphorylation increased with increasing amounts of stress. Intravenous administration of adrenaline increased SNAP-25 phosphorylation, although stress-induced phosphorylation was still observed in adrenalectomized mice. These results indicate that SNAP-25 phosphorylation is regulated in a stress-dependent manner through both central and peripheral mechanisms. We also investigated SNAP-25 dephosphorylation, and found that protein phosphatase 2A participates in SNAP-25 dephosphorylation through Ca2+-dependent and independent mechanisms.
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